RESUMO
To investigate the effects of TGF-ß1 on the proliferation and apoptosis of cervical cancer Hela cells in vitro. Human cervical cancer Hela cells were cultured in vitro and divided into the experimental and control groups. In the experimental groups, Hela cells were stimulated with different concentrations of TGF-ß1 (0.01, 0.1, 1, and 10 ng/mL), while Hela cells cultured in serum-free medium without TGF-ß1 were used as controls. The CCK8 method was adopted to detect the effect of TGF-ß1 on Hela cell proliferation, and flow cytometry was used to determine cell apoptosis 72 h after TGF-ß1 treatment. Compared with the control group, the CCK-8 tests showed that different concentrations of TGF-ß1 had no obvious effect on Hela cell proliferation 24 h after treatment (P > 0.05). However, upon 48 or 72 h of treatment, TGF-ß1 significantly inhibited the proliferation of Hela cells in a time- and dose-dependent manner (P < 0.05). The flow cytometry results indicated that TGF-ß1 influenced the apoptosis of human cervical cancer Hela cells in a dose-dependent manner after 72 h of treatment (P < 0.05). TGF-ß1 significantly inhibited the growth and induced the apoptosis of human cervical Hela cells in vitro.
Assuntos
Apoptose/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Fator de Crescimento Transformador beta/farmacologia , Células HeLa , HumanosRESUMO
OBJECTIVE: To investigate the effects of mTOR-STAT3 pathway on the invasion and migration of hepatoma cell. METHODS: mTOR and STAT3 expression in the hepatocellular carcinoma cell line HepG2 and normal liver cell line L02 were detected by reverse transcription PCR (RT-PCR) and western blotting. The migration and invasion abilities of cells and expression of STAT3 were detected by scratch adhesion test and transwell migration assays, after siRNA transfection blocking mTOR expression of HepG2 cells. RESULTS: The HepG2 cells expression is higher compared with normal cells L02 expression. Western blotting assay showed the mTOR expression was blocked, while STAT3 expression was also decreased, after the siRNA transfection of HepG2 cells. The migration (scratch adhesion test) and invasion (transwell assays) abilities of HepG2 cells which the mTOR expression was blocked by siRNA interference were significantly decreased (P<0.05). CONCLUSION: mTORSTAT3 expression in hepatoma cells HepG2 was significantly higher than that in normal liver cells. mTOR blocking can reduce the expression of STAT3, which is also closely related to the invasion and metastasis of liver cancer cells.