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@#Angiopoietin-like 4(ANGPTL4)is one of the angiopoietin family members and plays a regulatory role in lipid metabolism,glucose homeostasis,inflammatory signal transduction,angiogenesis and vascular permeability.Inflammatory reaction in tumor microenvironment regulates tumor progression,and tumor angiogenesis plays a vital role in tumor growth and metastasis,so ANGPTL4 is closely related to tumor occurrence and development.Many studies have shown that ANGPTL4 plays an important regulatory role in tumor growth,anoikis resistance,tumor angiogenesis and tumor metastasis.This paper reviews the role of ANGPTL4 in tumor progression.
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Objective: To investigate the effect of 1-acyl-sn-glycerol-3-phosphate acyltransferaseδ (APGAT4) on the growth and lenvatinib resistance of hepatocellular carcinoma (HCC), and provide novel targets for HCC treatment. Methods: Using the bioinformatics methods to screen out upregulated genes in lenvatinib resistant cell lines from GEO dataset and survival related genes from TCGA dataset. Immumohistochemical staining was used to detect the expression AGPAT4 in HCC tissues, and its correlation with patients' survival. CCK8, EdU, cell cycle, and cell apoptosis assays were used to investigate the impact of role AGPAT4 on the proliferation and lenvatinib reistance of HCC cells. AGPAT4 stable knockdown cell line and subcutaneous nude mouse model were established to test the therapeutic effects of Lenvatinib. Analysis of variance was used to compare the differences between data sets. Results: APGAT4 was the common factor that predicted poor survival and Lenvatinib resistance. The mRNA and protein levels of APGAT4 were significantly upregulated in HCC tissues compared to the para-tumor tissues (P < 0.05). Using siRNA could significantly knocked down the mRNA and protein expression of APGAT4 in HCC cell lines Hep3B and HCCLM3. Compared with the control group, the proliferation ability of HCC cell lines (Hep3B and HCCLM3) in APGAT4 knockdown group was significantly inhibited, and the cell cycle was arrested in G2/M phase (P < 0.05). In addition, compared to the control group, HCC cell lines (Hep3B and HCCLM3) in APGAT4 knockdown group showed significant decrease in the Lenvatinib half maximal inhibitory concentration, and were more sensitive to lenvatinib-induced apoptosis (P < 0.05). In HCC subcutaneous nude mouse model, compared to the control group, the growth of tumor in APGAT4 knockdown group was significantly suppressed, and more apoptosis cells were induced (P < 0.05). Conclusion: APGAT4 promotes the growth and Lenvatinib resistance of HCC, which is a potential target for HCC treatment. Targeting APGAT4 treatment is conducive to inhibit the growth and Lenvatinib resistance of HCC.
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Animals , Mice , Carcinoma, Hepatocellular/pathology , Liver Neoplasms/pathology , Mice, Nude , Cell Line, Tumor , Cell Proliferation , RNA, Messenger , Gene Expression Regulation, NeoplasticABSTRACT
Amygdalin is a potential therapeutically target in cancer. The main purpose of this experimental study was to evaluate the therapeutic effect of amygdalin in the mice model of breast cancer. The percentages of CD4, CD8 T lymphocyte, intracellular IFN-?, and Granzyme B were assessed in spleen cells of tumorized mice treated with 50 and 150 mg/kg of amygdalin (AG50 and AG150). The expression of caspase 3 and p53, tumor size, and survival rate of Balb/c mice was determined in tumor tissue after amygdalin administration. No significant difference was observed in the frequency of CD4+ and CD8+ T cells in the three study groups. However, a significantly increased level of granzyme B in CD8+ T cells, as well as a significant decrease in the level of IL-10 in CD4+ T cells was detected in the AG50 group compared to the AG150. There was no significant difference in the expression of caspase 3 and P53 between the two groups. A significant change was seen in tumor size and survival rate of AG50 and AG150 groups compared to the controls. Our findings indicated that antitumor effect of amygdalin in vivo was probably due to stimulating the effective immune response, not apoptotic genes induction
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SUMMARY: This study is to investigate the role and mechanism of RGD peptide in laryngeal cancer stem cells (CSCs). Laryngeal cancer CD133+Hep-2 CSCs were sorted by flow cytometry. RGD peptide was co-cultured with sorted laryngeal CSCs. Cell proliferation was detected with CCK-8 assay. The mRNA levels of VEGF/VEGFR2/STAT 3/HIF-1α were detected with RT-PCR. The proteins of VEGF/ VEGFR2/STAT 3/HIF-1α were detected with Western blot. The sorted CSCs were inoculated into nude mice. Tumor volume was measured. Integrin αvβ3 expression in tumor tissues was analyzed with immunohistochemistry. The results showed that the ratio of CD133+ CSCs to the total number of cells was 1.34±0.87 %, while CD133-non-tumor stem cells accounted for 95.0±5.76 %. The sorted cancer stem cells grew well. The RGD peptide significantly inhibited the proliferation of CD133+Hep-2 laryngeal CSCs in a dose-dependent manner. The RGD peptide significantly inhibited the mRNA of VEGFR2, STAT3 and HIF-1α in laryngeal CSCs in a concentration-dependent manner. Consistently, the RGD peptide significantly inhibited the protein expression of VEGFR2, STAT3 and HIF-1α in laryngeal CSCs in a dose-dependent manner. At the same time, in vivo tumor experiments showed that the RGD peptide significantly inhibited tumor volume but not the body weight. Furthermore, RGD peptide significantly inhibited the expression of tumor angiogenesis-related protein integrin αvβ3. Our findings demonstrate that RGD peptide inhibits tumor cell proliferation and tumor growth. The underlying mechanism may that RGD inhibits tumor angiogenesis-related signaling pathways, thus affecting the tumor angiogenesis, and decreasing the progression of human laryngeal CSCs.
Este estudio se realizó para investigar el papel y el mecanismo del péptido RGD en las células madre del cáncer de laringe (CSC). Las CSC CD133+Hep-2 de cáncer de laringe se clasificaron mediante citometría de flujo. El péptido RGD se cocultivó con CSC laríngeas clasificadas. La proliferación celular se detectó con el ensayo CCK-8. Los niveles de ARNm de VEGF/VEGFR2/ STAT 3/HIF-1α se detectaron con RT-PCR. Las proteínas de VEGF/ VEGFR2/STAT 3/HIF-1α se detectaron con Western blot. Las CSC clasificadas se inocularon en ratones nudos. Se midió el volumen del tumor. La expresión de integrina αvβ3 en tejidos tumorales se analizó con inmunohistoquímica. Los resultados mostraron que la proporción de CSC CD133+ con respecto al número total de células fue de 1,34 ± 0,87 %, mientras que las células madre no tumorales CD133 representaron el 95,0 ± 5,76 %. Las células madre cancerosas clasificadas crecieron bien. El péptido RGD inhibió significativamente la proliferación de CSC laríngeas CD133+Hep-2 de una manera dependiente de la dosis. El péptido RGD inhibió significativamente el ARNm de VEGFR2, STAT3 y HIF-1α en CSC laríngeas de manera dependiente de la concentración. De manera consistente, el péptido RGD inhibió significativamente la expresión proteica de VEGFR2, STAT3 y HIF-1α en CSC laríngeas, de manera dependiente de la dosis. Al mismo tiempo, los experimentos con tumores in vivo mostraron que el péptido RGD inhibía significativamente el volumen del tumor pero no el peso corporal. Además, el péptido RGD inhibió significativamente la expresión de la proteína integrina αvβ3 relacionada con la angiogénesis tumoral. Nuestros hallazgos demuestran que el péptido RGD inhibe la proliferación de células tumorales y el crecimiento tumoral. El mecanismo subyacente puede ser que RGD inhiba las vías de señalización relacionadas con la angiogénesis tumoral, afectando así la angiogénesis tumoral y disminuyendo la progresión de las CSC laríngeas humanas.
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Animals , Mice , Oligopeptides/metabolism , Neoplastic Stem Cells , Laryngeal Neoplasms , RNA, Messenger/antagonists & inhibitors , Immunohistochemistry , Blotting, Western , DNA Primers , Reverse Transcriptase Polymerase Chain Reaction , Integrin alphaVbeta3/antagonists & inhibitors , Vascular Endothelial Growth Factor A/antagonists & inhibitors , Vascular Endothelial Growth Factor A/genetics , Cell Proliferation , Flow Cytometry , Neovascularization, PathologicABSTRACT
Objective To establish a mathematical model of tumor growth and invasion under radiotherapy, so as to numerically simulate the effect of radiotherapy on tumor growth and make sensitivity analysis.Methods The mathematical model of tumor growth and invasion with time evolution before and after radiotherapy was established. The model included four key variables in the process of tumor invasion: tumor cells, extracellular matrix (ECM), matrix-degradative enzymes (MDEs) and oxygen. The linear quadratic (LQ) model was used to simulate the survival probability of tumor cells after radiotherapy, and the effects of different radiotherapy schemes and radiotherapy coefficients on the treatment effect were discussed. Traditional radiotherapy and intraoperative targeted radiotherapy were compared.Results Under the premise of constant total dose, the results of radiotherapy were directly proportional to the radiotherapy coefficient, but not related to the radiotherapy frequency; the therapeutic effect of intraoperative targeted radiotherapy was better than that of standard treatment.Conclusions Simulation results are basically consistent with clinical experimental results. As a more efficient treatment method, intraoperative targeted radiotherapy can provide new ideas for clinical tumor treatment.
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OBJECTIVE@#To explore the transcriptional regulation mechanism and biological function of low expression of vasoactive intestinal peptide receptor 1 (VIPR1) in hepatocellular carcinoma (HCC).@*METHODS@#We constructed plasmids carrying wild-type VIPR1 promoter or two mutant VIPR1 promoter sequences for transfection of the HCC cell lines Hep3B and Huh7, and examined the effect of AP-2α expression on VIPR1 promoter activity using dual-luciferase reporter assay. Pyrosequencing was performed to detect the changes in VIPR1 promoter methylation level in HCC cells treated with a DNA methyltransferase inhibitor (DAC). Chromatin immunoprecipitation was used to evaluate the binding ability of AP-2α to VIPR1 promoter. Western blotting was used to assess the effect of AP-2α knockdown on VIPR1 expression and examine the differential expression of VIPR1 in the two cell lines. The effects of VIPR1 overexpression and knockdown on the proliferation, cell cycle and apoptosis of HCC cells were analyzed using CCK8 assay and flow cytometry. We also observed the growth of HCC xenograft with lentivirus-mediated over-expression of VIPR1 in nude mice.@*RESULTS@#Compared with the wild-type VIPR1 promoter group, co-transfection with the vector carrying two promoter mutations and the AP-2α-over-expressing plasmid obviously restored the luciferase activity in HCC cells (P < 0.05). DAC treatment of the cells significantly decreased the methylation level of VIPR1 promoter and inhibited the binding of AP-2α to VIPR1 promoter (P < 0.01). The HCC cells with AP-2α knockdown showed increased VIPR1 expression, which was lower in Huh7 cells than in Hep3B cells. VIPR1 overexpression in HCC cells caused significant cell cycle arrest in G2/M phase (P < 0.01), promoted cell apoptosis (P < 0.001), and inhibited cell proliferation (P < 0.001), while VIPR1 knockdown produced the opposite effects. In the tumor-bearing nude mice, VIPR1 overexpression in the HCC cells significantly suppressed the increase of tumor volume (P < 0.001) and weight (P < 0.05).@*CONCLUSION@#VIPR1 promoter methylation in HCC promotes the binding of AP-2α and inhibits VIPR1 expression, while VIPR1 overexpression causes cell cycle arrest, promotes cell apoptosis, and inhibits cell proliferation and tumor growth.
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Animals , Humans , Mice , Carcinoma, Hepatocellular/pathology , Cell Line, Tumor , Cell Proliferation/genetics , Gene Expression Regulation, Neoplastic , Liver Neoplasms/pathology , Luciferases/genetics , Methylation , Mice, Nude , Receptors, Vasoactive Intestinal Polypeptide, Type I/metabolism , Transcription Factor AP-2/metabolismABSTRACT
Objective@#Cervical cancer (CC) is one of the most common malignant tumors in gynecology. This study aimed to investigate the prognostic significance of serum microRNA (miR)-378a-3p in CC and the effect of miR-378a-3p on tumor growth.@*Methods@#Real-time quantitative polymerase chain reaction analysis was used to measure the expression of miR-378a-3p in serum from patients with CC and healthy control subjects as well as from CC tissues and adjacent normal tissues. The association between serum miR-378a-3p levels and clinicopathological factors was analyzed. The correlation between miR-378a-3p levels and overall survival (OS) of CC patients was determined by Kaplan-Meier analysis. The CC cell proliferation and migration abilities after transfection of miR-378a-3p mimics were detected by Cell Counting Kit-8 and scratch wound healing assays, respectively. Tumor volume and weight in mice treated with miR-378a-3p were measured using a caliper and an electronic balance.@*Results@#MiR-378a-3p expression was downregulated in the serum and tissues of CC patients compared to that in healthy control subjects and normal tissues, respectively. Low expression of miR-378a-3p was positively correlated with large tumor size, advanced tumor stage, and lymph node metastasis. The OS of patients with low expression of miR-378a-3p was significantly lower than that of patients with high expression. Overexpression of miR-378a-3p suppressed the proliferation and migration of CC cells. @*Conclusion@#MiR-378a-3p downregulation is associated with the development and prognosis of CC, suggesting that it may be a potential biomarker for CC.
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Animals , Female , Humans , Mice , Middle Aged , Biomarkers/blood , Cell Movement , Cell Proliferation , Down-Regulation , Gene Expression Regulation, Neoplastic , Mice, Inbred BALB C , MicroRNAs/blood , Uterine Cervical Neoplasms/metabolismABSTRACT
Objective: To investigate the effect of toosendanin (TSN) on the growth and invasion of gastric cancer cells BGC-823 by regulating circDLST expression. Methods: After gastric cancer cells BGC-823 were exposed to different con-centrations of TSN (0, 0.5, 1.0, and 2.0 μmol/L) for 24 h, quantitative PCR was used to detect the expression of circDLST. BGC-823 cells were transfected with the circDLST overexpression lentiviral vector or its control vector (CON), and then treated with 0.5 μmol/L TSN or PBS. So the cells were divided into circDLST+TSN group, CON+TSN group and CON+PBS group. The viability and invasive potential of BGC-823 cells were observed by MTT proliferation test and Transwell invasion assay. The subcutaneous transplanted tumor models were established by using circDLST-transfected cell line BGC-823 or the control cell line in nude mice, and then 200 μg/kg TSN or the same volume of PBS was injected intraperitoneally every day. So the mice were divided into circDLST+TSN group, CON+TSN group and CON+PBS group. Results: Compared with the control group (0 μmol/L), all 3 concentrations of TSN decreased the expression levels of circDLST in a concentration dependent manner (P<0.01). TSN could significantly reduce the cell viability, cell invasion and subcutaneous xenograft tumor growth (P=0.000), while circDLST overexpression reversed the inhibitory effect of TSN (P<0.01). Conclusion: TSN may inhibit the growth and invasion of gastric cancer cells BGC-823 by downregulating circDLST expression.
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Objective To investigate the effect of medical sodium hyaluronate gel (HA) on the growth and metastasis of abdominal and pelvic tumor cells in vitro and in nude mice. Methods Three tumor cells, Hela, CT26 and HCT116, were used to investigate the effects of different HA concentrations on the growth and migration of tumor cells in vitro by MTT assay and Transwell assay. An orthotopic transplantation model of colonic tumor in nude mice was established to investigate the effect on the proliferation of cell HCT116 by comparing the tumor volume and tumor mass 4 weeks after inoculation. The effects on the metastasis of cell CT26 were investigated by comparing the tumor metastasis rate and the number of metastatic lesions of lung and liver in nude mice among the different experimental groups 3 weeks after inoculation. Results HA did not promote the growth and metastasis of Hela, CT26 and HCT116 cells in vitro at different concentrations. Actually, HA exhibited a certain inhibitory activity at the concentration of 5 mg/ml. In the orthotopic transplantation model of colonic tumor-HCT116, HA did not promote the growth of cell HCT116. In the orthotopic transplantation model of colonic tumor-CT26, HA inhibited CT26 tumor metastasis. Conclusion Under the experimental conditions, HA did not promote the growth, migration or metastasis of abdominal and pelvic related tumor cells including Hela, CT26 and HCT116 in vitro and in vivo.
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Reactive nitrogen species (RNS) affects intracellular redox balance and induces post-translational modification of proteins. Moreover, RNS, as the signal molecule, participates in the transduction of cellular signals under physiological conditions. However, excessive RNS can induce nitrosative stress and then damage cells, and thereby may play a role in the tumor initiation and progression. Thus, we discussed the role of RNS under physiological conditions and the tumor microenvironment, which may provide some novel ideas for the development of new drugs and the treatment of diseases.
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Chemotherapeutic drugs play an important role in the treatment of cancer, but the individual differences of patients' sensitivity to chemotherapeutic drugs and the drug resistance of chemotherapeutic drugs have always been a thorny problem in clinical treatment. Recent studies have shown that gut microbiota plays a key role in regulating the efficacy of chemotherapeutic drugs. Gut microbiota can regulate host response to chemotherapy through a variety of mechanisms, including immune interaction, heterogeneous metabolism and changes in community structure. This paper introduces the effects of traditional chemotherapeutic drugs and new immunotherapeutic drugs, such as anti-CTLA-4 and anti-PD-1 antibodies, on gut microbiota, as well as their effects on chemotherapeutic efficacy and mechanism, in order to provide evidences and clues for cancer treatments targeting gut microbiota.
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Objective To study the effect of intercellular adhesion of tumor cells on immune response of human body. Methods A tumor growth-cellular immune feedback model was developed based on cellular Potts model (CPM) to simulate the progression of tumor cells and the cellular immune feedback system, and the influence of adhesion between tumor cells on the immune system was analyzed. Results Under the condition of tumor intercellular adhesion with normal intensity, tumor cells could escape when the immune system was weak and be eliminated when the immune system was strong. Under the condition of tumor intercellular adhesion with low intensity, tumor cells could escape when the immune system was weak, while exhibited behavior of oscillation and could not be eliminated when the immune system was strong. Conclusions Higher adhesion between tumor cells inhibited escape of tumor cells from the immune system, while lower adhesion between tumor cells could effectively help the tumor escape killing from the immune system. When the tumor was extremely spread, the immune system could not completely eliminate tumor cells.
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Background: The suppression of cancer cell growth and invasion has become a challenging clinical issue. In this study, we used nanotechnology to create a new drug delivery system to enhance the efficacy of existing drugs. We developed layered double hydroxide by combing Au nanosol (LDH@Au) and characterized the compound to prove its function as a drug delivery agent. The anti-cancer drug Doxorubicin was loaded into the new drug carrier to assess its quality. We used a combination of apoptosis assays, cell cycle assays, tissue distribution studies, cell endocytosis, transwell invasion assays, and immunoblotting to evaluate the characteristics of LDH@Au as a drug delivery system. Results: Our results show that the LDH@Au-Dox treatment significantly increased cancer cell apoptosis and inhibited cell invasion compared to the control Dox group. Additionally, our data indicate that LDH@Au-Dox has a better target efficiency at the tumor site and improved the following: cellular uptake, anti-angiogenesis action, changes in the cell cycle, and increased caspase pathway activation. Conclusions: Our findings suggest the nano drug is a promising anti-cancer agent and has potential clinical applications.
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Stomach Neoplasms/drug therapy , Doxorubicin/administration & dosage , Apoptosis/drug effects , Nanoparticles/administration & dosage , Antibiotics, Antineoplastic/administration & dosage , Doxorubicin/pharmacology , Cell Cycle/drug effects , Blotting, Western , Drug Delivery Systems , Nanotechnology , Cell Line, Tumor , Microscopy, Electron, Transmission , Cell Proliferation/drug effects , Endocytosis/drug effects , Hydroxides , Antibiotics, Antineoplastic/pharmacology , Neoplasm Invasiveness/prevention & controlABSTRACT
Objective: To evaluate the effects of ropivacaine on cell proliferation and tumor growth of colon carcinoma. Methods: CCK8 assay was performed for cell viability. The colony formation assay was performed for cell proliferation. Cell flow apoptosis and cell cycle were measured by Flow cytometry. Protein levels were calculated by Western blot. Meanwhile,nude mice were inoculated with SW480 colon cells and treated with ropivacaine. Tumor volume and survival rate were examined after treatment. Results: The results of CCK8 showed that the optimum concentrations of ropivacaine were 20, 50 and 100 μg/ ml respectively. Ropivacaine dose-dependently inhibited colony formation (17. 80±0. 51,P<0. 001) and expressions of Ki67 (0. 32±0. 68, P<0. 01) and PCNA(0. 14±0. 24,P<0. 01). Meanwhile,treatment with ropivacaine markedly increased apoptosis (12. 80±1. 24,P< 0. 01) and protein levels of caspase-3(1. 76±1. 43,P <0. 001) and caspase-9 (1. 61±1. 26,P <0. 001) . In addition,ropivacaine notably induced cell cycle arrest (40. 5%,P<0. 01),expression of p53 (1. 16±0. 65,P<0. 01),and down-regulated the expression level of Cyclin A (0. 12±0. 12,P<0. 05) . Furthermore,ropivacaine inhibited tumor growth (1 247. 60±1. 37,P<0. 01),up-regulated survival rate of mice and induced apoptosis of tumor tissue (78. 00 ±1. 45,P <0. 001) in a dose-depended manner. Conclusion: Ropivacaine inhibits cell proliferation and tumor growth of colon cancer.
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Objective To investigate the therapeutic effects of Quercetin (QT)-loaded PLGA-TPGS nanoparticles (QPTN) on solid tumor-bearing mice with HCa-F hepatocarcinoma in vivo.Methods The model of HCa-F hepatocarcinoma solid tumor-bearing mice was established by implanting HCa-F cells into 48 mice.The mice were divided into 6 groups randomly:the negative control,empty PLGA-TPGS nanoparticles,5-Fluorouracil solutions (FS),Quercetin solutions (QTS),QT-loaded PLGA nanoparticles (QPN),and QPTN groups.Each group was treated using tail vein twice a day for 20 days;then,all mice were sacrificed.The increment tumor volumes and tumor growth inhibition rate were counted.Then,tumor specimens were prepared for hematoxylin & eosin (HE) staining and observed under a microscope.Results The results showed that the increment tumor volumes of mice in the QPTN,QPN,and FS groups were significantly smaller than that in the negative control group (P ＜ 0.05 or P ＜ 0.01).The tumor growth inhibition rate of the QPTN group was 59.07％,which was much higher than that of the QTS group (23.94％),the FS group (35.14％),and the QPN group (46.14％).The results of the HE staining on the tumor sections also indicated that the QPTN group showed a better therapeutic outcome compared to the other groups.Conclusion The QPTN has a better therapeutic effect on the model of solid tumor using HCa-F cells-bearing mice than the QPN,QTS,and FS.
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Objective The role of long non-coding RNA Linc00467 in human lung adenocarcinoma is not yet clear.This study was to investigate the expression of long non-coding RNA Linc00467 in human lung adenocarcinoma, its clinical significance, and the effects of Linc00467 on the functions of the tumor and endothelial cells in vitro.Methods Lung adenocarcinoma tissue and normal tissue surrounding the malignance were obtained from 60 patients with pathologically proved stage I-Ⅲa lung adenocarcinoma.Human umbilical vein endothelial cells (HUVECs) were transfected with the over-expressed plasmid pccl-Linc00467 (HUVEC experimental group) or the empty vector pccl (HUVEC control group), A549 cells with Linc00467-siRNA (A549 experimental group) or negative siRNA (A549 control group), and H1299 cells, too, with Linc00467-siRNA (H1299 experimental group) or negative siRNA (H1299 control group).The expression level of Linc00467 in the lung adenocarcinoma tissue was detected by qRT-PCR with an analysis of its correlation with the clinicopathological characteristics of the patients;the influence of Linc00467 on the proliferation of the A549, H1299 and HUVEC cells was assayed with CCK-8;and the role of Linc00467 in the angiogenesis of the HUVECs was assessed by fibrin bead sprouting assay.Results The expression of Linc00467 in the lung adenocarcinoma tissue was 2.72±1.31 times as high as that in the normal lung tissue (P<0.01), and those in the A549 and H1299 cells were 3.45±0.25 and 3.22±0.33 times as high as those in the human bronchial epithelial (HBE) cells (P<0.01).The expression level of Linc00467 was significantly correlated with the tumor size and vascular invasion (P<0.05).After transfection of Linc00467-siRNA, the expressions of Linc00467 in the A549 and H1299 experimental groups were down-regulated by 72% and 68% as compared with those in the A549 and H1299 control groups (P<0.01).The number of living cells was remarkably decreased in the A549 experimental group in comparison with the A549 control at 48 h (1.29±0.07 vs 1.51±0.09), 72 h (1.53±0.15 vs 2.13±0.11), and 96 h after culturing (1.98±0.18 vs 3.02±0.12), and so was it in the H1299 experimental versus the H1299 control group, but markedly increased in the HUVEC experimental versus the HUVEC control group (P<0.05).At 5 days, HUVEC experimental group, as compared with the HUVEC control, showed a significantly increased number of newly formed vascular branches (7.36 vs 4.25/superbead, P<0.01) and relative length of the blood vessels (3.12 vs 1, P<0.01).Conclusion Linc00467 promotes tumor cell proliferation and angiogenesis and is highly expressed in the lung adenocarcinoma tissue, which is correlated with the tumor size and vascular invasion and suggests that Linc00467 could be a potential biomarker and therapeutic target.
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Objective · To establish human cervical cancer xenografts in nude mice and investigate the antitumor therapeutic effects and safety of EGF modified cisplatin-alginate conjugate liposomes. Methods · Cervical cancer-bearing mouse model was established by subcutaneously injecting Hela cells in nude mice. Generalstate and xenograft growth of the mice were observed. Tumor volumes, tumor weights, and the body weights of mice during the treatment were recorded and analyzed. The expression levels of EGFR in xenografts were detected by immunohistochemistry. Results · ① EGFR was highly expressed in the xenografts. ② CS-EGF-Lip inhibited the tumor growth effectively (P=0.000). ③ The inhibition rates of tumor volume and tumor weight of CS-EGF-Lip were 80.22% and 58.60% respectively, which were betterthan those of cisplatin (P=0.000). ④ CS-EGF-Lip had minimal influence on body weight in mice (P=0.000). Conclusion · CS-EGF-Lip has more effective antitumoreffects than cisplatin in cervical cancer-bearing mice, which can inhibit tumor growth of solid tumors with enhanced efficacy and safety.
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Cancer cell metabolic reprogramming is a highly significant feature in tumor development and progression.This process is an extension of aerobic glycolysis(i.e.,Warburg effect).The metabolic pattern,such as that of glycolysis,oxidative phosphorylation, amino acid metabolism,fatty acid metabolism,and nucleic acid metabolism,is altered significantly during cell carcinogenesis.Fatty ac-id metabolism is required for energy storage,membrane proliferation,and signaling molecule generation.Thus,studying the mecha-nism of de novo fatty acid synthesis and its relationship with the development and progression of tumor,as well as the use and target-ing of the key enzyme in this metabolic pathway,is vital for the diagnosis,prevention,and treatment of cancer.Herein,we provide a brief review of metabolic reprogramming in cancer cells.We focus on the pathways of de novo fatty acid synthesis during the develop-ment and progression of tumor.
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Objective To explore the influence of Mac-1 deficiency on tumor growth of melanoma. Methods The population of Mac-1 gene knock-out ( Mac-1 -/ -) mice was expanded. B16-F10 cells were subcutaneously injected into the C57BL/6J mice (control group) and Mac-1 -/ -mice (experiment group), respectively. Subsequently,the survival rate, tumor volume and body weight were recorded. The proliferation and infiltration of macrophages were detected by immunohistochemistry. Results The survival rate of Mac-1 -/ - mice was significantly improved compared with the C57BL/6J mice (P ﹤0. 001). The tumor volume and body weight were remarkably decreased in the Mac-1 -/ - mice compared with the control group (P﹤0. 001). Meanwhile, the tumor cell proliferation index was decreased in the Mac-1 -/ - mice compared with the control group (P﹤0. 01). Furthermore, the infiltration of macrophages in the tumor tissues was also decreased in Mac-1 -/ - tumor mice compared with control group. Conclusions Mac-1 gene deletion can significantly suppress melanoma growth.
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Cancer cell metabolic reprogramming is a highly significant feature in tumor development and progression.This process is an extension of aerobic glycolysis(i.e.,Warburg effect).The metabolic pattern,such as that of glycolysis,oxidative phosphorylation, amino acid metabolism,fatty acid metabolism,and nucleic acid metabolism,is altered significantly during cell carcinogenesis.Fatty ac-id metabolism is required for energy storage,membrane proliferation,and signaling molecule generation.Thus,studying the mecha-nism of de novo fatty acid synthesis and its relationship with the development and progression of tumor,as well as the use and target-ing of the key enzyme in this metabolic pathway,is vital for the diagnosis,prevention,and treatment of cancer.Herein,we provide a brief review of metabolic reprogramming in cancer cells.We focus on the pathways of de novo fatty acid synthesis during the develop-ment and progression of tumor.