ABSTRACT
Aims To study the effects of diterpenoid pekinenal of Euphorbia pekinensis Rupr. on cell prolif-eration, cell cycle phase and apoptosis of hepatoma SMMC-7721 cells and to probe into its anti-cancer mechanisms. Methods MTT assay was used to inves-tigate the effect of pekinenal on proliferation of SMMC-7721 cells; TUNEL method, Annexin V/PI staining and electron microscopy were employed to observe the cell apoptosis; Flow cytometry was applied to analyze the distribution of cell cycle. Results Proliferation of SMMC-7721 cells was markedly inhibited by pekinenal in a dose-dependent manner; Annexin V/PI staining showed that with the increase of pekinenal concentra-tion, apoptotic rate of SMMC-7721 cells increased sig-nificantly, compared with control group, the difference has significant statistical significance ( P < 0. 01 ) . TUNEL method test results showed that different con-centrations of pekinenal in SMMC-7721 cells could in-duce liver cancer cell apoptotic and apoptotic index ( AI) increased significantly ( P <0. 01 ) with the in-crease of drug concentration. Compared with control group, electron microscope found that after the treat-ment, hepatocyte mitochondrial swelling, endoplasmic reticulum expansion, cytoplasm inclusion body forma-tion, part of the nucleus apoptosis, and the more obvi-ous apoptosis appeared with the increase of drug con-centration. Flow cytometry analysis showed that differ-ent concentrations of pekinenal could all make the cell block in S phase. Conclusion Pekinenal has an obvi-ously inhibitory effect on the human liver cancer cells, and there is significant concentration dependence; Pe-kinenal probably inhibits cancer cell DNA synthesis for the human liver cell cycle arrest in S phase and inhibits the proliferation . It plays a role in liver cancer inhibi-tion by inducing liver cancer cells apoptosis, etc.
ABSTRACT
Objective To study the effect of knockdown A20 expression on the proliferation, apoptosis and migra-tion of MCF-7 cells and to evaluate the potential value of the A20 gene as the therapeutic target of breast cancer. Methods Synthesized siRNA targeted to A20 gene or negative control siRNA were transfected into MCF-7 cells by using lipofectamine 2000. CCK8 assay, Annexin V and 7-AAD double staining cytometry, Transwell assay were performed to investigate the effect of knockdown A20 mRNA expression on the proliferation, apoptosis, migration of MCF-7 cells, respectively. Results It can inhibit the proliferation and migration as well as promote the apoptosis in MCF-7 cells by knockdown A20 mRNA expression. Conclusion A20 gene plays an important role in the prolif-eration, apoptosis and migration of MCF-7 cells and it could be a potential therapeutic target of breast cancer.
ABSTRACT
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.