AFP peptide (AFPep) as a potential growth factor for prostate cancer.

Prostate cancer is the most common cancer among men in the USA. A peptide derived from the active site of alpha-fetoprotein (AFP), known as AFPep, has been shown to be efficacious in inhibiting breast cancer growth. The role of this derived peptide AFPep in the development of prostate cancer has yet to be studied. To investigate the role of AFPep on prostate cancer, we used the PC-3 and DU-145 cell lines. We found that through key anti-apoptosis and pro-proliferation molecules, AFPep enhances the proliferation of DU-145 prostate cancer cells. The anti-proliferative molecules p18, p21, and p27, along with the pro-apoptotic molecules Fas and Bax, were all down-regulated in DU-145 cell lines treated with AFPep. Conversely, AFPep was not found to have a proliferative effect on the PC-3 prostate cancer cell line. This finding suggests the effects of AFPep to be cell line-specific in prostate cancer. Further investigation into the effects of AFPep could lead to new areas of treating prostate cancer.

Association between interleukin­33 and ovarian cancer.

Ovarian cancer is the leading cause of cancer­ associated mortality in the female reproductive system. Interleukin (IL)­33 and its receptor IL 1 receptor like 1 (also termed ST2) are expressed by many cell types including epithelial cells. The role of IL­33 in the pathogenesis of neoplasia remains controversial. The authors previously demonstrated that IL­33 inhibits the growth of pancreatic cancer cells. The present study was performed to explore if IL­33 has any direct effects on ovarian cancer cells. A clonogenic survival assay, immunohistochemistry (IHC), proliferation kit and caspase­3 activity kit were all used to evaluate the direct effects of IL­33 on cell proliferation and apoptosis of a widely studied ovarian cancer cell line, A2780. The possible molecular mechanisms were further evaluated with reverse transcription­polymerase chain reaction and IHC. It was demonstrated that the percentage of colonies and the optical density value of cancer cells were all increased in the presence of IL­33; however, the relative caspase­3 activity in cancer cells was decreased in the presence of IL­33. Molecular mechanism studies revealed that the pro­proliferative effect of IL­33 on cancer cells was associated with decreased levels of p27, and the anti­apoptotic effect of IL­33 was associated with levels of Fas cell surface death receptor (Fas) and tumor necrosis factor­related apoptosis­inducing ligand receptor 1 (TRAILR1). Therefore, IL­33 promoted proliferation and inhibited apoptosis of ovarian cancer cells by downregulation of p27, Fas and TRAILR1. Contrary to previous studies demonstrating an anti­tumor effort in pancreatic cancer, the results of the present study indicated that IL­33 exhibited a significant onco­promoting effect on ovarian cancer. Accordingly, the inhibition of IL­33 may be a promising therapeutic strategy for ovarian cancer.