Bafetinib inhibits ishikawa cells growth through modulating p16 expression

Abstract

Bafetinib is a tyrosine kinase inhibitor of Lyn- BCR/ABL that has been used experimentally for leukemia therapy. From our previous experimental work with bafetinib, it showed an anti-proliferative effect on Ishikawa cell line at concentration of 200nM. This observation was supported by colonogenic assay, the number of colonies formed by Ishikawa cells was 6 folds in the control comparing to bafetinib treated cells. Cells counting also support this finding, Ishikawa treated cells were unable to continue growing after 2 days of the drug addition comparing to the control cells that continued dividing. This underscores the role of bafetinib as anti-neoplastic agent on Ishikawa cells. To understand its mechanism of action, cyclin-dependent kinase inhibitors p16INK4a and p21 WAF1 that have major role in cell cycle arrest were measured. No difference was noticed in p21 levels between the treated and control cells; however, increasing in p16 expression was observed in treated Ishikawa cells. This underlines the role of bafetinib in inhibiting Ishikawa cells through modulating p16 expression. This suggests that bafetinib could be used as a therapy in case of endometrial cancer. But, further work should be conducted to examine the effect of bafetinib on other endometrial cancer cells and on mice before testing its effect on endometrial cancer patients.