Résumé
Aim To investigate the sensitization effect of total flavonoids of litchi seed (TFLS) to paclitaxel (PTX) on prostate cancer paclitaxel resistance (PCa-Txr) cells and the synergistic inhibitory effect of TFLS combined with PTX. Methods CCK-8 method was carried out to detect the inhibitory effect of TFLS and PTX on PCa-Txr cells as well as corresponding parental cells. PCa-Txr cells were either pre-treated or simultaneously treated with low cytotoxic dose of TFLS to observe the sensitivity of PCa-Txr cells to PTX. The synergistic inhibitory effect of TFLS combined with PTX on the proliferation of PCa-Txr cells were observed according to the method recommended by Chou T C. Combination index (CI) was used to determine whether TFLS and PTX had synergistic inhibitory effect. Results TFLS significantly inhibited the proliferation of PCa-Txr cells and parental cells in a certain time- and dose-dependent manner. The low dose of TFLS pre-treated or treated with PTX simultaneously failed to increase the sensitivity of PTX on PCa-Txr cells. TFLS combined with PTX significantly inhibited the proliferation of PCa-Txr cells with CI value less than one. Conclusions TFLS inhibits the proliferation of PCa-Txr cells, while TFLS combined with PTX has synergistic inhibitory effect on PCa-Txr cells. However, TFLS fails to increase the sensitivity of PCa-Txr cells to PTX.
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Aims: To investigate the differences and international connections between the human cervical cancer cell line (HeLa cells) and the Taxol-resistant HeLa cell line (HeLa/Taxol). Materials and Methods: As parental cells, HeLa cells were cultured in stepwise escalating concentration of Taxol from 0.01 μg/ml (11.7 × 10−9 mol/L) to 0.5 μg/ml (585 × 10−9 mol/L). The drug resistance of HeLa/Taxol cells was detected by methyl-thiazolyl-tetrazolium assay. Real time-polymerase chain reaction (RT-PCR) was conducted to detect the messenger RNA levels of drug resistance genes and apoptosis-related genes. The proteins levels were detected through immunofluorescence and Western blot. Results: Compared with parental HeLa cells, HeLa/Taxol with Taxol resistance had the following biological characteristics: first, they had a lower growth velocity; second, the expression of P-glycoprotein and glutathione S-transferases was significantly increased; Third, the expression of antiapoptotic protein Bcl-2 and apoptosis inhibitor protein survivin was prominently increased. Conclusions: The drug-resistance in HeLa/Taxol is mainly associated with the high expression of multidrug resistance genes, antiapoptotic protein Bcl-2, and apoptosis inhibitor protein survivin as an important reason for the failure of chemotherapy of tumor tissue
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Objective:To observe effect of ginsenoside Rh2 (GRh2) on the invasion and migration of colon cancer resistant cells HCT116/L-OHP and its specific mechanism. Method:Cell counting kit-8 (CCK-8) assay was used to detect the inhibitory effect of different concentrations of GRh2 (0, 2.5, 5, 10, 20, 40 mg·L-1) on HCT116/L-OHP cell proliferation, scratch assay, Transwell assay and adhesion assay were used to detect the effects of GRh2 (0, 2.5, 5, 10 mg·L-1) on cell migration, invasion and adhesion. The protein expression levels of E-cadherin and matrix metalloproteinase-9(MMP-9) were examined by Western blot. Result:Compared with control group, GRh2(5, 10, 20, 40 mg·L-1) significantly inhibited the proliferation of HCT116/L-OHP cells in a dose-dependent manner(PP2 group (5, 10 mg·L-1) was significantly decreased (PP2 group was significantly decreased (PP2 group was significantly reduced (PP2 (10, 20, 30 mg·L-1) promoted E-cadherin protein expression (PPPConclusion:GRh2 can significantly inhibit the invasion and migration of HCT116/L-OHP in colon cancer cells, and its potential mechanism may be related to the promotion of E-cadherin and the inhibition of MMP-9 expression in a dose-dependent manner.
Résumé
Aim To investigate the roles of FFJ-5 in human breast cancer MCF7 cells and drug-resistant MCF7/DOX cells and to explore its mechanisms. Methods MTT assay was used to detect the effect of FFJ-5 on MCF7 and MCF7/DOX cell proliferation and sensitivity of doxorubicin in MCF7/DOX cells.West-ern blot was used to investigate the effect of FFJ-5 on expression of EGFR,p-EGFR,Akt,p-Akt,PKM2, cleaved caspase-3,cleaved PARP and P-gp.DNA lad-der analysis was performed to determine the effect of FFJ-5 on genomic DNA.RT-PCR was performed to de-tect the influence of FFJ-5 on multidrug resistance gene MDR1 mRNA levels.Results The results showed that FFJ-5 inhibited the growth of MCF7 ,inhibited the expression and activity of EGFR and Akt,and conse-quently reduced the expression of PKM2 in MCF7 cells;FFJ-5 activated caspase-3 and induced genomic DNA fragmentation;FFJ-5 also inhibited the growth of MCF7/DOX cells and enhanced the anti-tumor activity of doxorubicin in MCF7/DOX cells.Conclusion The results suggest that FFJ-5 could inhibit MCF7 cell growth and induce MCF7 cell apoptosis through inhibi-tion of EGFR-Akt-PKM2 pathway and activation of ap-optosis-related factors caspase-3 , meanwhile FFJ-5 could also reverse the resistance of MCF7/DOX.