Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 22
Filtrar
Mais filtros










Intervalo de ano de publicação
1.
J Proteome Res ; 23(7): 2552-2560, 2024 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-38864484

RESUMO

Detection of exhaled volatile organic compounds (VOCs) is promising for noninvasive screening of esophageal cancer (EC). Cellular VOC analysis can be used to investigate potential biomarkers. Considering the crucial role of methionine (Met) during cancer development, exploring associated abnormal metabolic phenotypes becomes imperative. In this work, we employed headspace solid-phase microextraction-gas chromatography-mass spectrometry (HS-SPME-GC-MS) to investigate the volatile metabolic profiles of EC cells (KYSE150) and normal esophageal epithelial cells (HEECs) under a Met regulation strategy. Using untargeted approaches, we analyzed the metabolic VOCs of the two cell types and explored the differential VOCs between them. Subsequently, we utilized targeted approaches to analyze the differential VOCs in both cell types under gradient Met culture conditions. The results revealed that there were five/six differential VOCs between cells under Met-containing/Met-free culture conditions. And the difference in levels of two characteristic VOCs (1-butanol and ethyl 2-methylbutyrate) between the two cell types intensified with the increase of the Met concentration. Notably, this is the first report on VOC analysis of EC cells and the first to consider the effect of Met on volatile metabolic profiles. The present work indicates that EC cells can be distinguished through VOCs induced by Met regulation, which holds promise for providing novel insights into diagnostic strategies.


Assuntos
Neoplasias Esofágicas , Cromatografia Gasosa-Espectrometria de Massas , Metionina , Compostos Orgânicos Voláteis , Metionina/metabolismo , Compostos Orgânicos Voláteis/análise , Compostos Orgânicos Voláteis/metabolismo , Neoplasias Esofágicas/metabolismo , Neoplasias Esofágicas/patologia , Humanos , Cromatografia Gasosa-Espectrometria de Massas/métodos , Linhagem Celular Tumoral , Microextração em Fase Sólida , Células Epiteliais/metabolismo , Células Epiteliais/efeitos dos fármacos
2.
Asian Pac J Cancer Prev ; 25(4): 1433-1440, 2024 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-38680005

RESUMO

OBJECTIVE: aim of this study was to examine the synergistic effect between the antibacterial drug ciprofloxacin and the natural compound laetrile on esophageal cancer cells, specifically focusing on their combined cytotoxic effect. METHODS: The combined cytotoxic effects of two alternative incubation durations (24 and 72 hours) were studied using an esophageal cancer cell line.  Ciprofloxacin, laetrile, and their combinations were tested at concentrations ranging from 1 to 1000 micrograms/milliliter, to enhance the safety of the combination, the concentrations of the combination constituents were reduced by half compared to when they are used individually, the combination index was then calculated to estimate the components' possible synergistic effects. RESULT: The results indicate that the combined cytotoxicity of ciprofloxacin and laetrile was greater than the cytotoxicity of either ciprofloxacin or laetrile alone, the combination cytotoxicity increased with higher concentrations and longer incubation periods, in other words, the cytotoxicity pattern of the combination was time-dependent (cell-cycle specific), and concentration dependent, (cell-cycle non-specific). CONCLUSION: The study found that the combination of ciprofloxacin and laetrile had a greater inhibitory effect on the growth of esophageal cancer cells compared to ciprofloxacin or laetrile alone. This suggests a synergistic effect between the components of the mixture, which can be attributed to a complementary mechanism between the ingredients in the combination.


Assuntos
Proliferação de Células , Ciprofloxacina , Sinergismo Farmacológico , Neoplasias Esofágicas , Humanos , Ciprofloxacina/farmacologia , Neoplasias Esofágicas/tratamento farmacológico , Neoplasias Esofágicas/patologia , Proliferação de Células/efeitos dos fármacos , Ciclo Celular/efeitos dos fármacos , Células Tumorais Cultivadas , Apoptose/efeitos dos fármacos , Antibacterianos/farmacologia , Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
3.
Oncol Rep ; 50(1)2023 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-37203393

RESUMO

Increasing evidence showed that the substance P (SP)/neurokinin­1 receptor (NK1R) complex is involved in the development of several cancers. However, little is known about the mechanisms by which SP/NK1R complex plays a role in esophageal squamous cell carcinoma (ESCC) progression. RT­qPCR, CCK­8, Transwell, western blotting, immunohistochemical, immunofluorescence, ELISA and analysis of apoptosis were employed in the present study. It was aimed to investigate the function and therapeutic potential of the SP/tr­NK1R system in human ESCC progression. The results revealed that both SP and tr­NK1R were highly expressed in ESCC cell lines and specimens. In ESCC tissues, SP was mainly derived from ESCC cells and M2 macrophages. The NK1R antagonist aprepitant inhibited the SP­induced proliferation of human ESCC cell lines. Aprepitant inhibited cell migration and invasion and induced apoptosis of ESCC cells by downregulating the PI3K/AKT/mTOR signaling pathways. Animal experiments revealed that aprepitant inhibited tumor progression of ESCC in xenograft mice. In conclusion, high expression of SP plus tr­NK1R indicated poor prognosis in ESCC, suggesting that aprepitant has a potential application in ESCC. To the best of our knowledge, high SP and tr­NK1R expression in ESCC cell lines was reported for the first time in the present study. These findings provided evidence for a novel therapeutic strategy for patients with ESCC.


Assuntos
Neoplasias Esofágicas , Carcinoma de Células Escamosas do Esôfago , Humanos , Animais , Camundongos , Carcinoma de Células Escamosas do Esôfago/tratamento farmacológico , Carcinoma de Células Escamosas do Esôfago/genética , Carcinoma de Células Escamosas do Esôfago/metabolismo , Receptores da Neurocinina-1/genética , Receptores da Neurocinina-1/metabolismo , Aprepitanto/farmacologia , Neoplasias Esofágicas/tratamento farmacológico , Neoplasias Esofágicas/genética , Neoplasias Esofágicas/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Movimento Celular , Regulação Neoplásica da Expressão Gênica
4.
Eur J Pharmacol ; 921: 174669, 2022 Apr 15.
Artigo em Inglês | MEDLINE | ID: mdl-35248554

RESUMO

Esophageal cancer (EC) is one of the malignant cancer with pool survival due to the limited therapeutic and drug-resistance. Narciclasine, a natural compound from Lycoris sanguinea possesses antitumor and anti-inflammatory properties. However, the mechanisms underlying the growth-inhibitory effect of narciclasine against EC have not yet been elucidated. Experimental evidences indicated that narciclasine treatment significantly affected the distribution of FAK and its phosphorylation, resulting in proliferation inhibition and migration inhibition of EC. Our study also showed that narciclasine treatment triggered DNA damage and inhibited DNA replication, leading to cell cycle arrest and apoptosis. Further mechanistic studies indicated that narciclasine inhibited EC cell proliferation and migration through FAK/JNK and p38 pathway. Altogether, these findings suggest that narciclasine could be a potential novel chemotherapeutic agent for esophageal cancer cell proliferation and migration.


Assuntos
Alcaloides de Amaryllidaceae , Neoplasias Esofágicas , Alcaloides de Amaryllidaceae/farmacologia , Alcaloides de Amaryllidaceae/uso terapêutico , Apoptose , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Neoplasias Esofágicas/tratamento farmacológico , Humanos , Fenantridinas , Transdução de Sinais
5.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-932631

RESUMO

Objective:To evaluate the effect of circLPAR3 on the radiosensitivity of esophageal cancer cells and investigate its mechanism.Methods:The cancer tissues and and adjacent tissues of 37 patients with esophageal cancer were collected, and esophageal cancer cell lines Eca-109, EC9706 and KYSE30 and esophageal epithelial cells HET-1A were cultured in vitro. The expression levels of circLPAR3 and miR-1238 in the tissues and cells were measured by RT-qPCR. Eca-109 cells were transfected with circLPAR3 siRNA and miR-1238 mimics or co-transfected with circLPAR3 siRNA and miR-1238 inhibitor. Cell cloning experiment was conducted to evaluate the effects of silencing circLPAR3, overexpressing miR-1238, or silencing both circLPAR3 and miR-1238 on the radiosensitivity of Eca-109 cells. After Eca-109 cells that silenced circLPAR3, overexpressed miR-1238 or silenced both circLPAR3 and miR-1238 were exposed to 4 Gy irradiation, CCK-8 assay (A value), flow cytometry and Western blot were employed to assess the effects of silencing circLPAR3, overexpressing miR-1238, or silencing both circLPAR3 and miR-1238 combined with 4 Gy irradiation on the proliferation and apoptosis of Eca-109 cells and the expression levels of CyclinD1, p21, Bcl-2 and Bax proteins. Dual luciferase reporter gene experiment and RNA pull down experiment were performed to verify the regulatory relationship between circLPAR3 and miR-1238. Results:Compared with adjacent tissues, the expression level of circLPAR3 was up-regulated in the esophageal cancer tissues ( P<0.05), while that of miR-1238 was down-regulated ( P<0.05). Compared with HET-1A cells, the expression levels of circLPAR3 were up-regulated in the esophageal cancer cell lines Eca-109, EC9706 and KYSE30(all P<0.05), whereas those of miR-1238 were down-regulated (all P<0.05). Silencing circLPAR3 or overexpressing miR-1238 reduced the survival fraction of Eca-109 cells (all P<0.05), and the sensitization ratio was 1.21 and 1.75, respectively. Silencing circLPAR3 or overexpressing miR-1238 decreased the A value of Eca-109 cells and the expression levels of CyclinD1 and Bcl-2 proteins (all P<0.05), while increased the apoptosis rate of Eca-109 cells and the expression levels of p21 and Bax proteins (all P<0.05). After silencing circLPAR3 or overexpressing miR-1238 combined with 4 Gy irradiation, the A value of Eca-109 cells and the expression levels of CyclinD1 and Bcl-2 proteins were decreased (all P<0.05), while Eca-109 cell apoptosis rate and the expression levels of p21 and Bax proteins were increased (all P<0.05). circLPAR3 targeted and negatively regulated the expression level of miR-1238 in Eca-109 cells. After silencing miR-1238 and circLPAR3 simultaneously, the survival fraction of Eca-109 cells was higher than that when only silencing circLPAR3, and the sensitization ratio was 0.59. Silencing miR-1238 reversed the effects of silencing circLPAR3 combined with 4 Gy irradiation on the proliferation and apoptosis of Eca-109 cells. Conclusion:circLPAR3 is highly expressed in esophageal cancer tissues and cell lines, and silencing the expression of circLPAR3 can inhibit the proliferation of esophageal cancer Eca-109 cells, promote their apoptosis, and enhance cell radiosensitivity by up-regulating miR-1238.

6.
Acta Pharmaceutica Sinica ; (12): 793-801, 2022.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-922901

RESUMO

Multicellular tumor spheroids (MCTS) can simulate the structure and metabolic characteristics of tumors in vivo, which is of great significance to study the metabolic phenotype of tumor cells and the mechanism of drug intervention. In this study, esophageal cancer MCTS were constructed, and MCTS frozen sections were prepared after treated with different formulations of paclitaxel (PTX) including common PTX injection, PTX liposome and albumin bound PTX. MCTS mass spectrometry imaging analysis method was established by using air flow assisted desorption electrospray ionization mass spectrometry imaging (AFADESI-MSI). The visualization of the permeation and enrichment process of PTX in MCTs after PTX treatment was realized, and the spatially resolved metabolomics of PTX injection group was studied. The results showed that the permeation and enrichment behavior of PTX in MCTs model were related to the formulations. The changes of endogenous metabolites in MCTs of esophageal cancer after treated with PTX injection had temporal and spatial characteristics. The metabolic changes of MCTS during the initial 0-4 hours were dominated by the down-regulation of middle-high polarity metabolites and some lipids in the central region of MCTS, while the metabolic changes of MCTS during 8-72 hours were mainly up-regulated by lipid metabolites in the peripheral region of MCTS. The combination of in vivo tumor-associated MCTs model with label free, highly sensitive and high coverage mass spectrometry imaging technology provided a new method and strategy for the study of pharmacometabolomics.

7.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-910516

RESUMO

Objective:To examine the effect of FAM83D knockdown on proliferation, survival ability and invasion of human esophageal squamous cell carcinoma after X-ray radiation, and explore the mechanism.Methods:The expression of FAM83D, E-cadherin and vimentin in tumor tissues was detected in 69 cases of esophageal squamous cell cancer by using immunohistochemical method. The siRNA based on the sequences of the FAM83D mRNA were synthesized to transfect into the cultured ECA109 cells as FAM83D shRNA group. The effect of silencing FAM83D gene was evaluated to determine the protein levels of FAM83D in the human oesophageal squamous cell carcinoma ECA109 and KYSE30 cells using western blotting. MTS, clone formation, and Transwell assay were employed to examine the proliferation, survival ability and invasion of ECA109 and KYSE30 cells in vitro, respectively. We used flow cytometry assay to analyze distribution of cell apoptosis in different groups. Western blotting was used to examine the expression of cell metastasis-related molecules and apoptosis-related protein. Results:The strong expression rates of FAM83D, E-cadherin, and vimentin were 55%(38/69), 36%(25/69) and 61%(42/69) in the tumor tissues, respectively. FAM83D protein expression was significantly and negatively correlated with the expression of E-cadherin ( r=-0.350, P<0.01), and positively with the expression of vimentin ( r=0.470, P<0.01). Western blotting results demonstrated that silencing FAM83D gene significantly reduced the FAM83D protein expression ( P<0.01). MTS data demonstrated that FAM83D knockdown after irradiation significantly inhibited the proliferation of esophageal squamous cell carcinoma ECA109 and KYSE30 cells ( P<0.05). The data from the clone formation assay revealed that the radiosensitivity was increased after downragulation of FAM83D expression ( P<0.01). In addition, the invasive abilities of oesophageal carcinoma cells transfected with FAM83D shRNA after irradiation were significantly inhibited compared with those of the NC group ( P<0.01), followed by the downregulation of N-cadherin, vimentin, Snail, p-Akt and p-GSK-3β expression, and the upregulation of E-cadherin expression ( P<0.01). The apoptosis rate of tumor cells in FAM83D shRNA group after irradiation was markedly increased ( P<0.01), followed by a decrease of Bcl-2 and Mcl-1 expression and an increase of Cleaved caspase-3 expression ( P<0.01). Conclusions:FAM83D expressions was found to be closely related to the invasion and development of ESCC. Furthermore, siRNA interference technology inhibited the expression of FAM83D gene in oesophageal squamous cell carcinoma cells, reduced the proliferation, invasion of cells, induced cell apoptosis, and increased radiosensitivity, which may be associated with regulating the epithelial-mesenchymaltransition via Snail/Akt/GSK-3β signaling pathways.

8.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-910437

RESUMO

Objective:To clarify the role of classic Wnt signaling pathway in the radioresistance of esophageal cancer cells (ECC), and investigate the underlying mechanism, aiming to identify critical molecular targets for clinically enhancing the radiosensitivity of esophageal cancer.Methods:The radiosensitivity of four types of ECCs (EC9706, ECA109, KYSE70 and KYSE150) were assessed by colony formation assay. Western blot and RT-PCR were used to detect the activation of classical Wnt signaling pathway after irradiation. Classic Wnt signaling pathway activator (AZD2858) and inhibitor (XAV-939) were utilized to comprehensively evaluate the effect of classic Wnt signaling pathway on the radiosensitivity of ECCs. Cellular immunofluorescence staining was performed to detect the production and repair of DNA double-strand breaks (DSB), as well as the foci formation of DSB repair proteins after irradiation.Results:The results of colony formation assay showed that the radiosensitivity of four types of ECCs from high to low was EC9706, ECA109, KYSE70 and KYSE150. In KYSE150, a radioresistant cell type, the level of nuclear β-catenin and the transcription of c-Myc gene were significantly increased after irradiation (both P<0.05). However, in EC9706, a radiosensitive cell type, the level of nuclear β-catenin and c-Myc gene transcription were not affected by irradiation (both P>0.05). Moreover, EC9706 cells showed enhanced radioresistance in the presence of AZD2858( P<0.05), whereas XAV-939 treatment decreased the radioresistance in KYSE150 cells ( P<0.05). AZD2858 accelerated the DSB repair in EC9706 cells ( P<0.05), whereas XAV-939 delayed the DSB repair in KYSE150 cells ( P<0.05). Furthermore, the results of immunofluorescence staining showed that XAV-939 reduced the DSB repair capacity by inhibiting homologous recombination repair-related proteins (BRCA1 and RAD51) rather than non-homologous end junction repair-related proteins (Ku80 and XRCC4). Conclusions:The classic Wnt signaling pathway participates in the regulation of radiosensitivity in ECCs by regulating the homologous recombination repair of DSB after irradiation. Inhibition of the classic Wnt signaling pathway can counteract the radioresistance of ECCs and enhance the killing effect of irradiation on ECCs.

9.
Cells ; 8(10)2019 09 24.
Artigo em Inglês | MEDLINE | ID: mdl-31554233

RESUMO

The vacuolar H+-adenosine triphosphatase (ATPase) subunit V0C (ATP6V0C), a proton-conducting, pore-forming subunit of vacuolar ATPase, maintains pH homeostasis and induces organelle acidification. The intracellular and extracellular pH of cancer cells affects their growth; however, the role of ATP6V0C in highly invasive esophageal cancer cells (ECCs) remains unclear. In this study, we examined the role of ATP6V0C in glucose metabolism in ECCs. The ATP6V0C depletion attenuated ECC proliferation, invasion, and suppressed glucose metabolism, as indicated by reduced glucose uptake and decreased lactate and adenosine triphosphate (ATP) production in cells. Consistent with this, expression of glycolytic enzyme and the extracellular acidification rate (ECAR) were also decreased by ATP6V0C knockdown. Mechanistically, ATP6V0C interacted with pyruvate kinase isoform M2 (PKM2), a key regulator of glycolysis in ECCs. The ATP6V0C depletion reduced PKM2 phosphorylation at tyrosine residue 105 (Tyr105), leading to inhibition of nuclear translocation of PKM2. In addition, ATP6V0C was recruited at hypoxia response element (HRE) sites in the lactate dehydrogenase A (LDHA) gene for glycolysis. Thus, our data suggest that ATP6V0C enhances aerobic glycolysis and motility in ECCs.


Assuntos
Proteínas de Transporte/metabolismo , Neoplasias Esofágicas/metabolismo , Neoplasias Esofágicas/patologia , Glicólise/genética , Proteínas de Membrana/metabolismo , Hormônios Tireóideos/metabolismo , ATPases Vacuolares Próton-Translocadoras/fisiologia , Aerobiose/fisiologia , Movimento Celular/genética , Proliferação de Células/genética , Células Cultivadas , Neoplasias Esofágicas/genética , Células HeLa , Humanos , Invasividade Neoplásica , Fosforilação , Subunidades Proteicas/fisiologia , Transporte Proteico/genética , Transdução de Sinais/genética , Proteínas de Ligação a Hormônio da Tireoide
10.
Bioorg Chem ; 91: 103129, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31374522

RESUMO

Cyclopianes, featuring a highly rigid 6/5/5/5-fused tetracyclic framework, are structurally unique and biologically significant and belong to a rarely reported diterpenoid family. Chemical investigation of an EtOAc extract of a deep-sea-derived Penicillium sp. led to the isolation of three new cyclopiane diterpenes, namely, conidiogenols C-D (1-2) and conidiogenone L (3). The structures were determined by extensive analyses of the spectroscopic data in association with ECD calculations and chemical conversion for configurational assignments. Compound 1 represents the second example of cyclopianes bearing a hydroxyl group at C-13. Compound 2, the third example of conidiogenols, possesses a distinct α-oriented 1-hydroxy group relative to other analogues. The bioassay study demonstrated that compounds 2 and 4-6 exhibited moderate inhibitory effects against five esophageal cancer cell lines with IC50 values ranging from 25 to 55 µM. The cytotoxicities of all compounds toward esophageal cancer cell lines were evaluated for the first time.


Assuntos
Antineoplásicos/farmacologia , Carcinoma/tratamento farmacológico , Diterpenos/farmacologia , Neoplasias Esofágicas/tratamento farmacológico , Antineoplásicos/química , Antineoplásicos/isolamento & purificação , Linhagem Celular Tumoral , Diterpenos/química , Diterpenos/isolamento & purificação , Ensaios de Seleção de Medicamentos Antitumorais , Humanos , Estrutura Molecular , Penicillium/química , Relação Estrutura-Atividade
11.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-755081

RESUMO

Objective To evaluate the effect of GOLPH3 on the proliferation, apoptosis and radiosensitivity of OE33 esophageal cancer cell line. Methods The expression levels of GOLPH3 mRNA and protein in the esophageal cancer cells and normal esophageal epithelial cells were detected by qRT-PCR and Western blot, respectively. The OE33 esophageal cancer cells were transfected with GOLPH3 siRNA and subject to irradiation treatment simultaneously. The cell proliferation was detected by MTT assay. The cell apoptosis was detected by flow cytometry. The radiosensitivity was assessed by cell cloning test. The expression levels of cleaved Caspase-3, Bax and cleaved Caspase-9 protein levels were quantitatively measured by Western blot. Results The expression levels of GOLPH3 mRNA and protein in the esophageal cancer cells were significantly higher than those in the normal esophageal epithelial cells ( both P<0.05) . GOLPH3 siRNA could obviously down-regulate the expression levels of GOLPH3 mRNA and protein in the OE33 esophageal cancer cells. The proliferation activity of esophageal cancer cells was decreased, whereas the apoptosis rate was increased and the expression levels of cleaved Caspase-3, Bax and cleaved Caspase-9 were up-regulated after down-regulating the expression of GOLPH3 or irradiation treatment ( all P<0.05) . After down-regulating the expression of GOLPH3 in the esophageal cancer cells treated with irradiation, the cell proliferation activity was more significantly decreased, whereas the apoptosis rate was elevated and the expression levels of cleaved Caspase-3, Bax and cleaved Caspase-9 were more evidently up-regulated ( all P<0.05) . In the irradiated OE33 esophageal cancer cells after down-regulating the expression of GOLPH3, the radiosensitization ratio of the cells was 1.673. Conclusions GOLPH3 is highly expressed in the esophageal cancer cells. Down-regulating the expression of GOLPH3 can increase the radiosensitivity, induce the apoptosis and inhibit the proliferation of OE33 esophageal cancer cells.

12.
Chin J Integr Med ; 24(10): 763-767, 2018 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-29926388

RESUMO

OBJECTIVE: To investigate the anti-proliferative effects of saponins prepared from Plena Clematis (PC) cultured in Fujian Province, China on 4 human tumor cell lines and its possible anti-tumor mechanism. METHODS: The growth inhibition assays of saponins on human esophageal squamous carcinoma cell line (EC9706), human hepatoma cell line (HepG-2), human oral cancer cell line (KB) and human gastric cancer cell line (BGC-823) were evaluated in vitro by thiazolyl blue (MTT) method. The inhibitory effects on EC9706 treated with different concentrations of saponins (15.62, 31.25, 62.50, 125, 250 and 500 µg/mL) were performed in vitro by MTT method. The morphology and nuclear staining with acridine orange/ethidium bromide of EC9706 cells treated with saponins were illustrated under an inverted phase fluorescence microscope. The apoptotic effects of saponins were further evaluated by annexin-V/propidium iodide dual staining experiment to examine the occurrence of phosphatidylserine externalization onto the cell surface by a flflow cytometer. RESULTS: MTT assay showed that the saponins could inhibit the proliferation of 4 tumor cell lines. Among them, the maximum inhibition rate of 73.1% was detected in EC9706 cells at the saponins concentration of 250 µg/mL for 24 h. Further investigation indicated that the saponins induced EC9706 cells apoposis. The EC9706 cells presented apoptotic characteristics when treated with saponins, including that the morphologies of EC9706 cells were appeared round-shaped with higher refraction, and the cell nuclear stained orange with EB after 250 µg/mL saponins exposure. The flow cytometry analysis results showed that the induction of cell cycle arrest in apoptotic system may participate in the anti-proliferative activity of saponins on EC9706 cells. CONCLUSION: The saponins from PC exhibited significant cytotoxicity against human EC9706, KB, BGC-823, and HepG-2 cells and might be beneficial to development of ethnic pharmaceutical plant for potential anti-tumor drugs.


Assuntos
Antineoplásicos Fitogênicos/farmacologia , Clematis , Saponinas/farmacologia , Pontos de Checagem do Ciclo Celular/efeitos dos fármacos , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Clematis/química , Humanos
13.
Artigo em Inglês | WPRIM (Pacífico Ocidental) | ID: wpr-776639

RESUMO

OBJECTIVE@#To investigate the anti-proliferative effects of saponins prepared from Plena Clematis (PC) cultured in Fujian Province, China on 4 human tumor cell lines and its possible anti-tumor mechanism.@*METHODS@#The growth inhibition assays of saponins on human esophageal squamous carcinoma cell line (EC9706), human hepatoma cell line (HepG-2), human oral cancer cell line (KB) and human gastric cancer cell line (BGC-823) were evaluated in vitro by thiazolyl blue (MTT) method. The inhibitory effects on EC9706 treated with different concentrations of saponins (15.62, 31.25, 62.50, 125, 250 and 500 μg/mL) were performed in vitro by MTT method. The morphology and nuclear staining with acridine orange/ethidium bromide of EC9706 cells treated with saponins were illustrated under an inverted phase fluorescence microscope. The apoptotic effects of saponins were further evaluated by annexin-V/propidium iodide dual staining experiment to examine the occurrence of phosphatidylserine externalization onto the cell surface by a flflow cytometer.@*RESULTS@#MTT assay showed that the saponins could inhibit the proliferation of 4 tumor cell lines. Among them, the maximum inhibition rate of 73.1% was detected in EC9706 cells at the saponins concentration of 250 μg/mL for 24 h. Further investigation indicated that the saponins induced EC9706 cells apoposis. The EC9706 cells presented apoptotic characteristics when treated with saponins, including that the morphologies of EC9706 cells were appeared round-shaped with higher refraction, and the cell nuclear stained orange with EB after 250 μg/mL saponins exposure. The flow cytometry analysis results showed that the induction of cell cycle arrest in apoptotic system may participate in the anti-proliferative activity of saponins on EC9706 cells.@*CONCLUSION@#The saponins from PC exhibited significant cytotoxicity against human EC9706, KB, BGC-823, and HepG-2 cells and might be beneficial to development of ethnic pharmaceutical plant for potential anti-tumor drugs.


Assuntos
Humanos , Antineoplásicos Fitogênicos , Farmacologia , Pontos de Checagem do Ciclo Celular , Linhagem Celular Tumoral , Proliferação de Células , Clematis , Química , Saponinas , Farmacologia
14.
Eur J Pharmacol ; 815: 478-486, 2017 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-28800883

RESUMO

Jaridon 6, a novel ent-kaurene diterpenoid derived from Rabdosia rubescens (Hemsl.) Hara, possesses strong anti-tumor activity in esophageal cancer cells. In this study, we explored the underlying molecular events of the anti-tumor activity of Jaridon 6. Cell viability and apoptosis results obtained by flow cytometry confirmed the tumor inhibitory effect of Jaridon 6 in esophageal cancer cells. A cDNA microarray was performed and the observations were validated using quantitative reverse transcription polymerase chain reaction. The microarray data showed that 151 genes were differentially expressed between the untreated group and the Jaridon 6-treated group, among these were 57 upregulated genes, and 94 downregulated genes (P < 0.01, fold change threshold: 2). These included genes such as Wnt, peroxisome, and genes involved in chemokine signaling pathways. In addition, Western blot analysis demonstrated that Jaridon 6 regulated the expression of Wnt pathway proteins, including reduced levels of Dvl 2, survivin and cyclin D1, and increased levels of p-ß-catenin, and AXIN2 in EC109 and EC9706 esophageal cancer cells. In addition, recombinant murine Wnt3a could change the regulation of Jaridon 6 on Wnt pathway proteins. Immunohistochemical analysis indicated that the anti-tumor activity of Jaridon 6 was closely related to the Wnt signaling pathway in esophageal cancer cells.


Assuntos
Antineoplásicos/farmacologia , Diterpenos do Tipo Caurano/farmacologia , Neoplasias Esofágicas/patologia , Transcriptoma/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Apoptose/genética , Linhagem Celular Tumoral , Humanos , Via de Sinalização Wnt/efeitos dos fármacos , Via de Sinalização Wnt/genética
15.
Oncol Lett ; 13(4): 2805-2810, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28454470

RESUMO

Terrein is a bioactive fungal metabolite isolated from Aspergillus terreus. Besides being a melanogenesis inhibitor, previous studies have revealed that terrein has antiproliferative effects on a number of types of cancer tumors. In the present study, the inhibitory effect of terrein on esophageal cancer was evaluated and the possible underlying mechanisms were investigated. The results revealed that terrein inhibited the proliferation of Eca109 esophageal cancer cells in a dose- and time-dependent manner. Mechanistically, terrein treatment led to the G2/M phase arrest of Eca109 cells by indirectly regulating cyclin B1 and phosphorylating the cell division cycle protein 2 genes. Notably, terrein exhibited a synergistic effect on Eca109 cells when combined with cisplatin, which is a commonly used chemotherapeutic drug. Taken together, these findings indicate that terrein suppresses the proliferation of esophageal cancer cells, and may prove to be a novel therapeutic approach for the treatment of esophageal cancer via inhibiting the proliferation of cancer cells.

16.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-508107

RESUMO

Objective Early clinical symptoms of esophageal cancer are often not obvious , so a deeper insight into tumor markers is very important for the early diagnosis of esophageal cancer .This study was to investigate the expressions of Rock 2 and Wnt11 in the specific esophageal cancer cell lines Eca-109 and HEEC and the relationship of the signal transduction pathway of proteins with the development of esophageal cancer . Methods Esophageal cancer cell lines Eca-109 and HEEC were cultured and the expression levels of Rock2 and Wnt11 in the cell lines were determined by real-time quantitative PCR and Western blot . Results The mRNA expressions of Rock2 and Wnt11 were significantly increased in the Eca-109 as compared with those in the HEEC cell line (4.955± 0.539 vs 1.000±0.000, P<0.01;2.925±0.230 vs 1.000±0.000, P<0.01), and so were the protein expressions of Rock 2 and Wnt11 (955.000±21.628 vs 778.844±102.193, P<0.05;2175.316±145.623 vs 1312.233±50.734, P<0.05). Conclusion The up-regula-ted expressions of Rock 2 and Wint11 may be the markers of the metastasis of esophageal squamous cancer .

17.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-505195

RESUMO

Objective To establish a radioresistant esophageal squamous cancer cell line,and to identify the radioresistant genes and mechanisms.Methods The radioresistant KYSE410-res cell line was established by repeated exposure of cell line KYSE410 to radiation.The proliferation and apoptosis of esophageal squamous cancer cells were evaluated before and after radiation.The changes in gene expression of the esophageal squamous cancer cells after radiation were determined by gene microarray and analyzed by group t test.The genes with significant difference in expression after radiation were validated.Results The KYSE410-res cells had significantly enhanced proliferation and anti-apoptosis than the KYSE410 cells (all P<0.05).The result of gene microarray showed that compared with the KYSE410 cells,the KYSE410-res cells had the expression of 463 and 251 genes upregulated and downregulated by no less than 4 folds,respectively.Those genes with different expression levels after radiation were mainly responsible for cell proliferation,adhesion,signal transduction,angiogenesis,reactive oxygen metabolism,cell damage repair,and the MAPK/ERK signaling pathway.OAS2 and UBD were key proteins in the network.In the KYSE410-res cells,the expression of HLA-DQBI,MMP1,NCAM1,ZNF521,GPC6,SELENBP1,LCN15,and TFPI-2 genes measured by real-time PCR was consistent with that measured by gene microarray.Conclusions Abnormal activation of the MAPK/ERK signaling pathway,upregulated expression of OAS2 and UBD,downregulated expression of TFPI-2,and upregulated expression of MMPs may play a role in radioresistance of esophageal cancer cells.

18.
Mol Clin Oncol ; 4(4): 599-602, 2016 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-27073672

RESUMO

The present study evaluated the capture efficiency of esophageal and breast cancer cells with a modified 'polymeric circulating tumor cells (CTC)-chip' microfluidic device, which was developed for the isolation of circulating tumor cells. Esophageal cancer cell lines KYSE150, KYSE220 and KYSE510, and breast cancer cell lines MCF7, SKBR3 and MDA-MB-231 were used for evaluation. The capture efficiencies of the esophageal cancer cell lines in phosphate-buffered saline (PBS) were ~0.9, irrespective of epithelial cell adhesion molecule (EpCAM) expression, which was represented as the mean fluorescent intensity from 528 to 76. In the breast cancer cell lines, efficient capture was observed for MCF7 and SKBR3 in PBS; however, a low value of ~0.1 was obtained for MDA-MB-231. Fluorescent imaging of immunolabeled cells revealed marginal EpCAM expression in MDA-MB-231. Using whole blood, no clogging occurred in the microstructure-modified CTC-chip and efficiency of capture was successfully evaluated. Capture efficiencies for KYSE220 and MCF7 in whole blood were >0.7, but were of either equal or lesser efficiency in comparison to PBS. Therefore, the modified CTC-chip appears useful for clinical application due to its cost, practicality of use, and efficient cancer cell capture.

19.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-459997

RESUMO

Objective To explore and analyze the effects of allicin prodrug on proliferation of esophageal cancer cell line Eca9706 and the expression of apoptosis gene.Methods Different concentrations of allicin prodrugs were divided into a total of four groups:A1 group(10μg/mL),A2 group(20 μg/mL),A3 group (40 μg/mL),A4 group (normal saline,0 μg/mL),and respectively applicated in esophageal carcinoma cell line Eca9706.After culturing for 1 days,2 days,3 days,cell proliferation was detected by MTT and expression of p53 at the mRNA level was detected by RT-PCR.Results The optimum concentration of proliferation inhibition of allicin prodrug on esophageal cancer cell line Eca9706 was 20μg/mL and the best inhibition time was 2 days;the gene level of esophageal cancer cell line Eca9706 was inhibited with a dose-dependent.Conclusion Allicin prodrugs could effectively inhibit the proliferation of esophageal cancer cell line Eca9706,and control the proliferation of esophageal cancer cells by regulating the expression of apoptosis associated genes,so as to eliminate tumor cells.

20.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-855283

RESUMO

Objective: To investigate the inhibition of luteoloside on the proliferation of human esophageal carcinoma cell line Eca109 and its mechanism. Methods: MTT assay was used for detecting the influence of luteoloside at different concentration on the proliferation of Eca109. The morphological changes of cells were observed under inverted microscope. The cell cycle and apoptosis were detected by flow cytometry. RT-PCR was used to detect the mRNA expression of cyclin D1, survivin, and c-myc genes. Results: The results of MTT assay showed different doses (80, 120, 160, 200, and 240 μmol/L) of luteoloside could inhibit the cell proliferation of Eca109 cells in a dose-response manner. Luteoloside could also change the morphological characteristics of cells, reduce the cell size, and separate from peripheral cells. Treated with 240 μmol/L luteoloside, the cells were sprouting and some of them developed multiple pseudopodia-like protrusions. Treated with luteoloside (160 and 240 μmol/L), the cell cycle of Eca109 cells was blocked in G2/M phase and apoptosis was induced (P < 0.05). Compared with the control group, the gene expression of cyclin D1, survivin, and c-myc was decreased after treated with 240 μmol/L luteoloside for 48 h (P < 0.05). Conclusion: Luteoloside could significantly inhibit the proliferation of Eca109 cells by changing the cell cycle and inducing the apoptosis. Moreover, it could decrease the mRNA expression of relative genes.

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...