Activin A increases the proliferation of OVCAR-3 ovarian cancer cells, potentially through the bcl-2 anti-apoptosis pathway.
Activin A-bcl-2 signaling may drive ovarian cancer cell growth; leaves open therapeutic targeting in patients.
To investigate the proliferation effect and its pathway of activin A on Ovarian epithelial cancer cells line OVCAR-3. OVCAR-3 cells were cultured in vitro and the membrane receptor ActR II was detected by immunohistochemical method. The OVCAR-3 cells were cultured with 10 ng/ml activin A for 7 d to observe the effects. Activin A at 5, 10, 15 and 20 ng/ml was used separately to treat the OVCAR-3 cancer cells for 24, 48 and 72 h in order to draw the growth proliferation rate curve measured by MTT method. The expression of protein bcl-2 was detected by western-blot. When OVCAR-3 cells were treated with 10 ng/ml activin A and 5 μg/ml DDP for 24, 48 and 72 h, cell apoptosis could be detected by electron microscopy and flow cytometry (FCM). Positive expression of ActR II was detected. We also found that the proliferation of OVCAR-3 reached to the climax on the 5th day of culture. The experiments showed that the cells treated with activin A increased quickly and grew faster than those in control group. Moreover, OVCAR-3 cells treated with activin A for 48 h proliferated significantly greater than those treated for 24 h or 72 h ( P <0.01). bcl-2 protein expression increased expression in activin A treated group than in control group ( P <0.05). Activin A could increase the proliferation of OVCAR-3 cells which may be through bcl-2 anti-apoptosis pathway.
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Li et al. (2008) studied this question.
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