Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 1.655
Filter
3.
Int. braz. j. urol ; 47(1): 93-99, Jan.-Feb. 2021. tab, graf
Article in English | LILACS | ID: biblio-1134320

ABSTRACT

ABSTRACT Hypothesis: Endoclip can be used as fiducial marker in urology. Objective: To assess the feasibility, cost effectiveness and reliability of endoclips as novel fiducial markers in precision radiotherapy, as part of a trimodality bladder-preserving treatment (TBPT) of muscle-invasive bladder carcinoma. Materials and Methods: This retrospective study was performed at Weifang People's Hospital (Weifang, China) from January 2015 to June 2018. A total of 15 patients underwent TBPT. Endoclips were applied to healthy edges of the resected bladder wall as novel fiducial markers. Radio-sensitizing chemotherapy and routine precision radiotherapy were given. The number and position of the endoclips during radiotherapy sessions were monitored. Complications and tumor recurrence were analyzed. Results: The mean age (±standard deviation) of the patients was 67±10 years (range 46-79). There were 3 females and 12 males. Forty-nine endoclips were applied in all patients (3.3±0.8). The tumor was completely visibly resected in all patients. The number of endoclips remained the same through the planned last radiotherapy session (3.3±0.8), i.e., none were lost. All endoclips were removed after the last radiotherapy session. The average number of follow-up months was 38.9±13.2 (range 11-52). There were no procedure-related complications at discharge or follow-up. At one-year, overall recurrence-free survival was 93.3%. Two patients had recurrences at 18 months and 10 months after TBPT, respectively, and salvage radical cystectomy was performed with no further recurrences. Another patient died due to metastasis 9 months after the completion of therapy. Conclusions: Endoclips are reliable, safe and cost-effective as novel fiducial markers in precision-radiotherapy post-TBPT.


Subject(s)
Humans , Male , Female , Aged , Urinary Bladder Neoplasms/surgery , Urinary Bladder Neoplasms/radiotherapy , Carcinoma , Urinary Bladder , Cystectomy , China , Feasibility Studies , Reproducibility of Results , Retrospective Studies , Treatment Outcome , Combined Modality Therapy , Fiducial Markers , Middle Aged , Muscles , Neoplasm Invasiveness , Neoplasm Recurrence, Local
4.
Braz. j. med. biol. res ; 54(2): e9017, 2021. graf
Article in English | LILACS, ColecionaSUS | ID: biblio-1142574

ABSTRACT

The purpose of this study was to investigate the anti-cancer effect of melittin on growth, migration, invasion, and apoptosis of non-small-cell lung cancer (NSCLC) cells. This study also explored the potential anti-cancer mechanism of melittin in NSCLC cells. The results demonstrated that melittin suppressed growth, migration, and invasion, and induced apoptosis of NSCLC cells in vitro. Melittin increased pro-apoptotic caspase-3 and Apaf-1 gene expression. Melittin inhibited tumor growth factor (TGF)-β expression and phosphorylated ERK/total ERK (pERK/tERK) in NSCLC cells. However, TGF-β overexpression (pTGF-β) abolished melittin-decreased TGF-β expression and pERK/tERK in NSCLC cells. Treatment with melittin suppressed tumor growth and prolonged mouse survival during the 120-day observation in vivo. Treatment with melittin increased TUNEL-positive cells and decreased expression levels of TGF-β and ERK in tumor tissue compared to the control group. In conclusion, the findings of this study indicated that melittin inhibited growth, migration, and invasion, and induced apoptosis of NSCLC cells through down-regulation of TGF-β-mediated ERK signaling pathway, suggesting melittin may be a promising anti-cancer agent for NSCLC therapy.


Subject(s)
Animals , Rabbits , Apoptosis , Carcinoma, Non-Small-Cell Lung/genetics , Carcinoma, Non-Small-Cell Lung/drug therapy , MAP Kinase Signaling System , Lung Neoplasms/genetics , Lung Neoplasms/drug therapy , Melitten/pharmacology , Down-Regulation , Gene Expression Regulation, Neoplastic , Cell Movement , Transforming Growth Factor beta/metabolism , Cell Line, Tumor , Caspase 3 , Apoptotic Protease-Activating Factor 1 , Neoplasm Invasiveness
5.
Braz. j. med. biol. res ; 54(2): e10394, 2021. tab, graf
Article in English | LILACS | ID: biblio-1153512

ABSTRACT

MicroRNAs (miRNAs) have been indicated to be frequently dysregulated in various cancers and promising biomarkers for colon cancer. The present study aimed to assess the prognostic significance and biological function of miR-1273a in colon cancer. The expression levels of miR-1273a was estimated using quantitative real-time polymerase chain reaction. Kaplan-Meier survival curves and Cox regression analysis were used to evaluate the prognostic value of miR-1273a in patients of colon cancer. The effects of miR-1273a on cell proliferation, migration, and invasion were investigated by cell experiments. The expression of miR-1273a was downregulated in colon cancer tissues and tumor cell lines compared with the normal controls (all P<0.001). The aberrant expression of miR-1273a was associated with vascular invasion (P=0.005), differentiation (P=0.023), lymph node metastasis (P=0.021), and TNM stage (P=0.004). The patients with low miR-1273a expression had low overall survival compared with the patients with high miR-1273a expression (log-rank P=0.002). miR-1273a was detected to be an independent prognostic biomarker for patients. Furthermore, the results of cell experiments revealed that miR-1273a downregulation promoted, while miR-1273a upregulation suppressed the cell proliferation, migration, and invasion. In conclusion, all data indicated that a downregulated expression of miR-1273a predicted poor prognosis for colon cancer and enhanced tumor cell proliferation, migration, and invasion. Thus, we suggest that methods to promote miR-1273a expression may serve as novel therapeutic strategies in colon cancer.


Subject(s)
Humans , Male , Female , Middle Aged , Colonic Neoplasms/diagnosis , MicroRNAs/genetics , Biomarkers, Tumor/genetics , Cell Movement/genetics , Colonic Neoplasms/genetics , Cell Proliferation/genetics , Neoplasm Invasiveness
6.
Braz. j. med. biol. res ; 54(2): e9161, 2021. graf
Article in English | LILACS | ID: biblio-1153511

ABSTRACT

Patients with osteosarcoma (OS) usually have poor overall survival because of frequent metastasis. Long non-coding RNAs (lncRNAs) have been reported to be associated with tumorigenesis and metastasis. In this study, we investigated the expression and roles of lncRNA human histocompatibility leukocyte antigen (HLA) complex P5 (HCP5) in OS, aiming to provide a novel molecular mechanism for OS. HCP5 was up-regulated both in OS tissues and cell lines and high expression of HCP5 was associated to low survival in OS patients. Down-regulation of HCP5 inhibited cell proliferation, migration, and invasion, suggesting its carcinogenic role in OS. miR-101 was targeted by HCP5 and its expression was decreased in OS. The inhibitor of miR-101 reversed the impact of HCP5 down-regulation on cell proliferation, apoptosis, and metastasis in OS. Ephrin receptor 7 (EPHA7) was proved to be a target of miR-101 and had ability to recover the effects of miR-101 inhibitor in OS. In conclusion, lncRNA HCP5 knockdown suppressed cell proliferation, migration, and invasion, and induced apoptosis through depleting the expression of EPHA7 by binding to miR-101, providing a potential therapeutic strategy of HCP5 in OS.


Subject(s)
Humans , Bone Neoplasms/genetics , Bone Neoplasms/pathology , Osteosarcoma/genetics , Osteosarcoma/pathology , MicroRNAs/metabolism , RNA, Long Noncoding/genetics , Down-Regulation , Gene Expression Regulation, Neoplastic , Cell Movement , Receptor, EphA7/metabolism , Cell Line, Tumor , Cell Proliferation , Neoplasm Invasiveness
8.
Article in English | WPRIM | ID: wpr-878451

ABSTRACT

OBJECTIVES@#The effect of isoprenylcysteine carboxymethyltransferase (ICMT) silencing on the migration and invasion of tongue squamous cell carcinoma was investigated by constructing the small interfering RNA (siRNA) of ICMT.@*METHODS@#Through liposomal transfection, siRNA was transfected into human tongue squamous cell carcinoma CAL-27 and SCC-4 cells (ICMT-siRNA group) with a negative control group (transfected with NC-siRNA) and a blank control group (transfected with a transfection reagent but not with siRNA). Quantitative real-time polymerase chain reaction was performed to analyze the mRNA expression of ICMT and RhoA in each group of cells after transfection and to measure the silencing efficiency. Western blot was applied to examine the expression levels of ICMT, total RhoA, membrane RhoA, ROCK1, matrix metalloproteinase (MMP)-2, and MMP-9 proteins in each group. The migration and invasion abilities were evaluated via wound healing and Transwell motility assays.@*RESULTS@#After CAL-27 and SCC-4 cells were transfected with ICMT-siRNA, the expression levels of ICMT genes and proteins decreased significantly in the experimental group compared with those in the negative and blank control groups (@*CONCLUSIONS@#The migration and invasion abilities of CAL-27 and SCC-4 cells were reduced significantly after the transfection of ICMT-siRNA, and the involved mechanism might be related to the RhoA-ROCK signaling pathway.


Subject(s)
Carcinoma, Squamous Cell , Cell Line, Tumor , Cell Movement , Cell Proliferation , Humans , Neoplasm Invasiveness , Protein Methyltransferases , RNA, Small Interfering , Tongue , Tongue Neoplasms , Transfection , rho-Associated Kinases
9.
Article in English | WPRIM | ID: wpr-878413

ABSTRACT

OBJECTIVES@#A study was conducted to investigate the molecular mechanism of chromodomain helicase/ATPase DNA binding protein 1-like gene (CHD1L) influencing the invasion and metastasis of tongue squamous cell carcinoma and to provide a new target for clinical inhibition of invasion and metastasis of tongue squamous cell carcinoma.@*METHODS@#Ualcan website was used to analyze the expression of CHD1L in normal epithelial tissue and primary head and neck squamous cell carcinoma and to analyze the effect of lymph node metastasis on the expression of CHD1L in tissues with head and neck squamous cell carcinoma. The relationship between CHD1L expression and the survival rate of patients with head and neck squamous cell carcinoma was tested by the GEPIA website. Western blot was used to quantify the levels of CHD1L protein in human tongue squamous cell carcinoma CAL27 and immortalized human skin keratinocyte cell HaCaT. After knocking down CAL27 in human tongue squamous cell carcinoma cells with an RNA interference plasmid, the cells were designated as SiCHD1L/CAL27 and Scr/CAL27. Western blot was utilized to detect the expression of CHD1L in each group of cells. The change in CAL27 cell proliferation ability was tested by EdU proliferation test after CHD1L knockdown. The change of cell migration ability of each group cells was tested through the wound healing assay. Western blot was used to detect epithelial-mesenchymal transition (EMT) marker E-cadherin and Vimentin protein expression levels.@*RESULTS@#Ualcan database showed that the expression of CHD1L in primary head and neck squamous cell carcinoma tissues was higher than in normal epithelial tissues and in head and neck squamous cell carcinoma tissues with lymph node metastasis. GEPIA website analysis showed that the overall survival rate of patients with head and neck squamous cell carcinoma with high expression of CHD1L was significantly lower than that of patients with low expression. Western blot results showed that CHD1L expression in human tongue squamous carcinoma cells CAL27 was higher than that of human normal skin cells HaCaT. CHD1L expression in SiCHD1L/CAL27 cells was much lower than that in Scr/CAL27 cells. Results of EdU proliferation experiments showed the significant reduction in the cell proliferation ability of the SiCHD1L/CAL27 cells. Results of the wound healing experiments showed the reduction in the migration capacity of the SiCHD1L/CAL27 cells. The expression of E-cadherin increased, whereas that of Vimentin decreased, in SiCHD1L/CAL27 cells.@*CONCLUSIONS@#CHD1L promoted the EMT, proliferation, migration, and invasion ability of tongue squamous cell carcinoma cells.


Subject(s)
Adenosine Triphosphatases , Carcinoma, Squamous Cell/genetics , Cell Line, Tumor , Cell Movement , Cell Proliferation , DNA Helicases , DNA-Binding Proteins , Epithelial-Mesenchymal Transition , Gene Expression Regulation, Neoplastic , Head and Neck Neoplasms , Humans , Neoplasm Invasiveness/genetics , Tongue , Tongue Neoplasms/genetics
10.
Article in English | WPRIM | ID: wpr-878331

ABSTRACT

Objective@#The underlying mechanism of Ezrin in ovarian cancer (OVCA) is far from being understood. Therefore, this study aimed to assess the role of Ezrin in OVCA cells (SKOV3 and CaOV3) and investigate the associated molecular mechanisms.@*Methods@#We performed Western blotting, reverse transcription-quantitative polymerase chain reaction, MTT, cell colony, cell wound healing, transwell migration and invasion, RhoA and Rac active pull down assays, and confocal immunofluorescence experiments to evaluate the functions and molecular mechanisms of Ezrin overexpression or knockdown in the proliferation and metastasis of OVCA cells.@*Results@#The ectopic expression of Ezrin significantly increased cell proliferation, invasiveness, and epithelial-mesenchymal transition (EMT) in OVCA cells. By contrast, the knockdown of endogenous Ezrin prevented OVCA cell proliferation, invasiveness, and EMT. Lastly, we observed that Ezrin can positively regulate the active forms of RhoA rather than Rac-1 in OVCA cells, thereby promoting robust stress fiber formation.@*Conclusion@#Our results indicated that Ezrin regulates OVCA cell proliferation and invasiveness by modulating EMT and induces actin stress fiber formation by regulating Rho-GTPase activity, which provides novel insights into the treatment of the OVCA.


Subject(s)
Cell Line, Tumor , Cell Movement , Cell Proliferation , Cytoskeletal Proteins/metabolism , Epithelial-Mesenchymal Transition , Female , Gene Expression Regulation, Neoplastic , Humans , Neoplasm Invasiveness , Ovarian Neoplasms/pathology , Stress Fibers/metabolism , rhoA GTP-Binding Protein/metabolism
11.
Int. braz. j. urol ; 46(6): 950-961, Nov.-Dec. 2020. graf
Article in English | LILACS | ID: biblio-1134248

ABSTRACT

ABSTRACT Objective To evaluate the effects of Arf6 downregulation on human prostate cancer cells. Materials and Methods The effects of Arf6 downregulation on cell proliferation, migration, invasion and apoptosis were assessed by MTT, BrdU, scratch, Transwell assays and flow cytometry respectively. AKT, p-AKT, ERK1/2, p-ERK1/2 and Rac1 protein expressions were detected by Western blot. Results Downregulating Arf6 by siRNA interference suppressed the mRNA and protein expressions of Arf6. The proliferation capacities of siRNA group at 48h, 72h, and 96h were significantly lower than those of control group (P <0.05). The migration distance of siRNA group at 18h was significantly shorter than that of control group (P <0.01). The number of cells penetrating Transwell chamber membrane significantly decreased in siRNA group compared with that of control group (P <0.01). After 24h, negative control and normal control groups had similar apoptotic rates (P >0.05) which were both significantly lower than that of siRNA group (P <0.01). After Arf6 expression was downregulated, p-ERK1/2 and Rac1 protein expressions were significantly lower than those of control group (P <0.05). Conclusion Downregulating Arf6 expression can inhibit the proliferation, migration and invasion of prostate cancer cells in vitro, which may be related to ERK1/2 phosphorylation and Rac1 downregulation.


Subject(s)
Humans , Male , Prostatic Neoplasms/genetics , Down-Regulation , Gene Expression Regulation, Neoplastic , Cell Movement , Apoptosis , RNA, Small Interfering/genetics , Cell Line, Tumor , Cell Proliferation , Neoplasm Invasiveness
12.
Int. braz. j. urol ; 46(2): 169-184, Mar.-Apr. 2020. tab, graf
Article in English | LILACS | ID: biblio-1090578

ABSTRACT

ABSTRACT Background Standard management of muscle-invasive bladder cancer involves radical cystectomy with pelvic lymph node dissection. However, patients may be ineligible for surgery or may wish to avoid the morbidity of cystectomy due to quality of life concerns. Bladder preservation therapies have emerged as alternatives treatment options that can provide comparable oncologic outcomes while maintaining patients' quality of life. Objective To review bladder preservation therapies, patient selection criteria, and functional and oncologic outcomes for BPT in muscle-invasive bladder cancer. Materials and Methods We conducted a comprehensive literature review of bladder preservation therapies in Pubmed and Embase. Discussion The ideal patient for BPT has low-volume T2 disease, absence of CIS, absence of hydronephrosis, and a maximal TURBT with regular surveillance. Technological advancements involving cancer staging, TURBT technique, and chemotherapy and radiation therapy regimens have improved BPT outcomes, with oncologic outcomes now comparable to those of radical cystectomy. Advancements in BPT also includes a heightened focus on improving quality of life for patients undergoing bladder preservation. Preservation strategies with most evidence for use include trimodality therapy and partial cystectomy with pelvic lymph node dissection. Conclusions This review highlights the breadth of strategies that aim to preserve a patient's bladder while still optimizing local tumor control and overall survival. Future areas for innovation include the use of predictive biomarkers and implementation of immunotherapy, moving the field towards patient-tailored care.


Subject(s)
Humans , Urinary Bladder Neoplasms/surgery , Cystectomy/methods , Urinary Bladder Neoplasms/pathology , Combined Modality Therapy , Organ Sparing Treatments , Neoplasm Invasiveness , Neoplasm Staging
13.
Rev. argent. coloproctología ; 31(1): 2-7, mar. 2020. tab, ilus
Article in Spanish | LILACS | ID: biblio-1100300

ABSTRACT

Introducción: El budding tumor (BT) es la presencia de células tumorales aisladas o en pequeños grupos situadas en el frente de invasión del tumor. Su hallazgo en alto grado es un factor de mal pronóstico independiente del cáncer colorrectal. El objetivo de este trabajo es determinar si el grado de BT está asociado con otros factores pronósticos del cáncer rectal. Material y métodos: Se incluyen las resecciones oncológicas de recto en el período 2013-2017. Los casos se agruparon según la densidad en la formación de los BT en 3 grupos, los de grado bajo, intermedio y alto. Se utilizó como valor estadístico el cálculo del odds ratio (OR). Resultados: Se analizaron las piezas de resección de 27 pacientes (15 mujeres y 12 hombres) con una media de edad de 68,4 años (40-86). Se calculó el OR para invasión ganglionar, vascular y recidiva en función del grado de budding tumoral. Discusión: Se observó una tendencia a la presencia de factores histológicos de mal pronóstico en relación al budding de alto grado, si bien el bajo número de casos no permitió demostrarlo en este estudio. Conclusiones: El análisis del grado de tumor budding es reproducible y podría ayudar a identificar pacientes con cáncer rectal de peor pronóstico. (AU)


Introduction: Tumor budding (BT) is defined as isolated or small groups of neoplastic cells located at the invasive front of the tumor. High-grade BT is a poor prognostic factor in colorectal cancer. Objective: To determine if the degree of BT is associated with other prognostic factors in rectal cancer. Materials and methods: Rectal oncological resections during the 2013-2017 period were included. Cases were stratified according to the density in the formation of BT in 3 groups: low, intermediate and high. The calculation of the odds ratio (OR) was used as a statistical value. Results: The resection specimens of 27 patients (15 women and 12 men) with a mean age of 68.4 years (40-86) were analyzed. OR for node metastases, vascular invasion and relapse was calculated according to tumor budding grade. Discussion: High-grade tumor budding seems to associate with the presence of poor prognostic factors. However, it was not possible to demonstrate it because of the small sample size. Conclusions: Tumor budding is a reproducible marker and could help to identify rectal cancer patients with a worse prognosis. (AU)


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Aged, 80 and over , Rectal Neoplasms/pathology , Adenocarcinoma/pathology , Prognosis , Rectal Neoplasms/surgery , Adenocarcinoma/surgery , Statistical Analysis , Retrospective Studies , Follow-Up Studies , Neoplasm Invasiveness/pathology , Neoplasm Staging
14.
Rev. Assoc. Med. Bras. (1992) ; 66(2): 210-215, Feb. 2020. graf
Article in English | LILACS, SES-SP | ID: biblio-1136186

ABSTRACT

SUMMARY OBJECTIVES Lymphomas are a heterogeneous set of malignant neoplasias of lymphoid B and NK/T mature and immature cells at various stages of differentiation. Genetic and molecular biology tools are used to appropriately classify the type and prognosis of the lymphomas, which have implications in therapeutic effectiveness. Among them, the nicotinamide adenine dinucleotide phosphate-oxidase (NADPH) oxidase (NOX5) enzymes have been explored. This study analyzed the expression of NADPH oxidase 5 in lymphoma tissue according to the degree of tumor aggressiveness. METHODS Slides from 64 patients with lymphoma who had paraffin-embedded tissue available were reviewed by two independent, experienced pathologists. They classified tumors according to the WHO classification (2017). NOX5 expression in tissues was assessed by immunohistochemical staining using a tissue microarray. The assay was interpreted using a scoring system of 0, 1, 2, and 3, for cytoplasmic staining of NOX5 corresponding to negative, weak, intermediate, and strong staining, respectively. We compared the expression of NOX5 in patients with aggressive versus non-aggressive lymphomas. RESULTS NOX5 expression was positive in 100% (27/27) of aggressive lymphomas and in 19% (7/37) of non-aggressive ones. The seven patients with positive expression of NOX5 presented intermediate staining (2); strong staining (3) was observed only in tissues of aggressive lymphomas, and negative and weak staining (0 and 1) were observed only in non-aggressive lymphomas. CONCLUSIONS Aggressive lymphomas overexpress NOX5 protein. The higher NOX5 expression in aggressive lymphomas can suggest an involvement of this enzyme on the acquisition of an aggressive phenotype in lymphoid neoplasia.


RESUMO OBJETIVOS Os linfomas são um grupo heterogêneo de neoplasias malignas de células linfoides B e NK/T maduras e imaturas em vários estágios de diferenciação. Ferramentas de biologia molecular e genética são usadas para classificar adequadamente o tipo e o prognóstico dos linfomas, os quais têm implicações na eficácia terapêutica. Entre eles, as enzimas nicotinamida adenina dinucleótido fosfato oxidase (NADPH) oxidase (NOX5) foram exploradas. Este estudo analisou a expressão da NADPH oxidase 5 em linfomas de acordo com o grau de agressividade tumoral. MÉTODOS As lâminas de 64 pacientes com linfoma, que tinham tecido embebido em parafina disponível, foram revisadas por dois patologistas experientes independentemente. Eles utilizaram a classificação da OMS (2017). A expressão de NOX5 nos tecidos foi avaliada por coloração imuno-histoquímica utilizando microarray de tecido. O ensaio foi interpretado com um sistema de pontuação de 0, 1, 2 e 3, para coloração citoplasmática de NOX5 correspondente à coloração negativa, fraca, intermediária e forte, respectivamente. Comparamos a expressão de NOX5 em pacientes com linfomas agressivos versus não agressivos. RESULTADOS A expressão de NOX5 foi positiva em 100% (27/27) dos linfomas agressivos e em 19% (7/37) dos linfomas não agressivos. Os sete pacientes com expressão positiva de NOX5 apresentaram coloração intermediária (2); coloração forte (3) foi observada apenas em tecidos de linfomas agressivos, e negativos e fracos (0 e 1) observados apenas em linfomas não agressivos. CONCLUSÕES Linfomas agressivos superexpressam a proteína NOX5. A expressão aumentada de NOX5 em linfomas agressivos pode sugerir um envolvimento dessa enzima na aquisição de um fenótipo agressivo na neoplasia linfoide.


Subject(s)
Humans , Up-Regulation , NADPH Oxidase 5/analysis , Lymphoma/pathology , Prognosis , Immunohistochemistry , Retrospective Studies , Paraffin Embedding , Neoplasm Invasiveness
15.
Säo Paulo med. j ; 138(1): 60-63, Jan.-Feb. 2020. tab
Article in English | LILACS | ID: biblio-1099382

ABSTRACT

ABSTRACT BACKGROUND: Transcatheter arterial chemoembolization (TACE) is thought to prevent recurrence of hepatocellular carcinoma (HCC), but its efficacy is a matter of controversy. OBJECTIVES: We investigated the effect of preventive TACE on the tumor, nodes, metastasis (TNM) classification in cases of stage II HCC (T2N0M0) after R0 resection. DESIGN AND SETTING: Case-control study conducted in a tertiary-level public hospital. METHODS: We analyzed recurrence rates and mortality rates over time for 250 consecutive cases of HCC in TNM classification cases of stage II HCC (T2N0M0) after R0 resection. These cases were divided into patients who underwent TACE (TACE+) and presented microvascular invasion (MVI+; n = 80); TACE+ but did not present MVI (MIV−; n = 100); MVI+ but did not undergo TACE (TACE−, n = 30); and TACE−/MVI− (n = 40). RESULTS: MVI+ patients in the TACE+ group had significantly lower recurrence rates and mortality rates at one, two and three years than those in the TACE- group (all P < 0.05). Among MVI- patients, the TACE+ group did not have significantly lower recurrence rates and mortality rates at one, two and three years than the TACE- group (all P > 0.05). Regardless of whether TACE was performed or not, MVI− patients had significantly lower recurrence rates and mortality rates at two and three years after their procedures than did MVI+ patients (all P < 0.05). CONCLUSION: Recurrence rates and mortality rates for MVI+ patients were significantly higher than for MVI− patients, beyond the first year after TACE. Postoperative adjuvant TACE may be beneficial for HCC patients with MVI.


Subject(s)
Humans , Chemoembolization, Therapeutic , Carcinoma, Hepatocellular , Liver Neoplasms , Case-Control Studies , Retrospective Studies , Neoplasm Invasiveness , Neoplasm Recurrence, Local
16.
Braz. j. med. biol. res ; 53(7): e9029, 2020. graf
Article in English | LILACS, ColecionaSUS | ID: biblio-1132531

ABSTRACT

This study examined the expression and potential mechanism of microRNA (miRNA)-424-5p in nasopharyngeal carcinoma (NPC). NPC tissues were collected from 40 patients who were enrolled in the study, and skin samples were collected from 26 healthy subjects during plastic surgery as controls. We performed various in vitro assays using miR-424-5p to examine its function in primary NPC-1 cells. Bioinformatics was employed to analyze potential target genes and signaling pathways of miR-424-5p. We found that miR-424-5p expression in NPC tissues is downregulated and negatively correlated with lymph node metastasis and clinical staging. Expression of miR-424-5p in NPC cells was also downregulated, and transfection with miR-424-5p mimics inhibited proliferation, migration, and invasion of NPC-1 cells. Bioinformatics identified the AKT3 gene as a potential target of miR-424-5p and dual luciferase assays confirmed this finding. Upregulation of AKT3 expression rescued the inhibitory effect of miR-424-5p on the proliferation, migration, and invasion. Our results suggest that miR-424-5p inhibited the proliferation, migration, and invasion of NPC cells by decreasing AKT3 expression.


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Gene Expression Regulation, Neoplastic , Nasopharyngeal Neoplasms/metabolism , MicroRNAs/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Nasopharyngeal Carcinoma/metabolism , Signal Transduction , Cell Movement , Nasopharyngeal Neoplasms/genetics , Blotting, Western , MicroRNAs/genetics , Cell Line, Tumor , Cell Proliferation , Proto-Oncogene Proteins c-akt/genetics , Real-Time Polymerase Chain Reaction , Nasopharyngeal Carcinoma/genetics , Neoplasm Invasiveness
17.
Acta Physiologica Sinica ; (6): 235-242, 2020.
Article in Chinese | WPRIM | ID: wpr-827064

ABSTRACT

Gliomas are malignant tumors with strong invasiveness. The current treatment strategy is surgical treatment assisted by a variety of radiotherapies, chemotherapies and immunotherapies. However, the curative efficacy is limited. Adrenergic receptor (AR) is an important stress hormone receptor, which is highly involved in the regulation of the tumorigenesis and progression of various tumors by activating different downstream signal transduction pathways. Recent studies have shown that AR is dysregulated in glioma cells and tissues, and plays an important role in a series of biological behaviors such as tumorigenesis, invasion and metastasis of glioma. This article reviews the research progress of AR in the field of glioma in recent years, which provides a theoretical basis for the prevention and treatment of glioma targeting the AR.


Subject(s)
Brain Neoplasms , Pathology , Carcinogenesis , Cell Line, Tumor , Cell Proliferation , Gene Expression Regulation, Neoplastic , Glioma , Pathology , Humans , Neoplasm Invasiveness , Neoplasm Metastasis , Receptors, Adrenergic , Physiology , Signal Transduction
18.
Protein & Cell ; (12): 825-845, 2020.
Article in English | WPRIM | ID: wpr-880875

ABSTRACT

This study was designed to evaluate ERK5 expression in lung cancer and malignant melanoma progression and to ascertain the involvement of ERK5 signaling in lung cancer and melanoma. We show that ERK5 expression is abundant in human lung cancer samples, and elevated ERK5 expression in lung cancer was linked to the acquisition of increased metastatic and invasive potential. Importantly, we observed a significant correlation between ERK5 activity and FAK expression and its phosphorylation at the Ser


Subject(s)
A549 Cells , Animals , Cell Movement , Epithelial-Mesenchymal Transition/genetics , Focal Adhesion Kinase 1/metabolism , Humans , Lung Neoplasms/pathology , MAP Kinase Signaling System , Mice , Mitogen-Activated Protein Kinase 7/metabolism , Neoplasm Invasiveness , Neoplasm Metastasis , Neoplasm Proteins/metabolism
19.
Article in Chinese | WPRIM | ID: wpr-880802

ABSTRACT

OBJECTIVE@#To investigate the effect of miR-4443 expression on migration and invasion of breast cancer.@*METHODS@#We examined the expression of miR-4443 in breast carcinoma in situ and paired adjacent tissues from 3 breast cancer patients with high-throughput sequencing and verified the results using TCGA database. We also detected miR-4443 expressions using real-time quantitative PCR (RT-qPCR) in low invasive and highly invasive breast cancer cells (MCF-7 and MDA-MB-231 cells, respectively). The changes in apoptosis, migration and invasion of MCF-7 and MDA-MB-231 cells after transfection with miR-4443 mimics, mimics-NC, miR-4443 inhibitor or inhibitor-NC were analyzed using flow cytometry, wound healing assay and Transwell invasion assay. The target gene of miR-4443 was predicted by bioinformatics software and validated by a dual luciferase reporter gene system. RT-qPCR and Western blotting were performed to detect the expression of recombinant human phosphatidyl ethanolamine binding protein 1 (PEBP1) in the transfected cells.@*RESULTS@#The expression of miR-4443 was significantly higher in the breast cancer tissues than in the adjacent tissues (@*CONCLUSIONS@#MiR-4443 promotes the migration and invasion of breast cancer cells by inhibiting the expression of PEBP1, suggesting the possibility of suppressing miR-4443 expression as a potential therapeutic strategy for breast cancer.


Subject(s)
Breast Neoplasms/genetics , Cell Line, Tumor , Cell Movement , Cell Proliferation , Gene Expression Regulation, Neoplastic , Humans , MCF-7 Cells , MicroRNAs/genetics , Neoplasm Invasiveness/genetics , Phosphatidylethanolamine Binding Protein
20.
Braz. j. med. biol. res ; 53(4): e8882, 2020. tab, graf
Article in English | LILACS | ID: biblio-1100927

ABSTRACT

Hepatocellular carcinoma (HCC) is one of the most common primary malignant tumors of the liver worldwide. Liver resection and transplantation are currently the only effective treatments; however, recurrence and metastasis rates are still high. Previous studies have shown that the epithelial-mesenchymal transition (EMT) is a key step in HCC invasion and metastasis. Inhibition of EMT has become a new therapeutic strategy for tumors. Recently, puerarin, a well-characterized component of traditional Chinese medicine, has been isolated from Pueraria radix and exerts positive effects on many diseases, particularly cancers. In this study, CCK-8, EdU immunofluorescence, colony formation, wound healing, and migration assays were used to detect the effects of puerarin on HCC cells. We further analyzed the relationship between puerarin and miR-21/PTEN/EMT markers in HCC cell lines. Our results showed that HCC cell proliferation, migration, invasion, tumor formation, and metastasis were reduced by puerarin in vitro and in vivo. Additionally, puerarin inhibited the EMT process of HCC by affecting the expression of Slug and Snail. Moreover, oncogenic miR-21 was inhibited by puerarin, coupled with an increase in the tumor suppressor gene PTEN. Increasing miR-21 expression or decreasing PTEN expression reversed the inhibition effects of puerarin in HCC. These data confirmed that puerarin affects HCC through the miR-21/PTEN/EMT regulatory axis. Overall, puerarin may represent a chemopreventive and/or chemotherapeutic agent for HCC treatment.


Subject(s)
Animals , Male , Carcinoma, Hepatocellular/drug therapy , PTEN Phosphohydrolase/genetics , Epithelial-Mesenchymal Transition/drug effects , Isoflavones/therapeutic use , Liver Neoplasms/drug therapy , Antineoplastic Agents/therapeutic use , Pyrroles , Drug Screening Assays, Antitumor , Carcinoma, Hepatocellular/genetics , MicroRNAs/genetics , Cell Proliferation/drug effects , Cell Proliferation/genetics , Disease Models, Animal , Isoflavones/pharmacology , Liver Neoplasms/genetics , Neoplasm Invasiveness , Antineoplastic Agents/pharmacology
SELECTION OF CITATIONS
SEARCH DETAIL