Down-regulation of anti-apoptosis protein livin promotes HMR1275 (flavopiridol)-induced apoptosis of endometrial carcinoma cell line ishikawa

HMR1275 (flavopiridol) is one of the commonly used drugs for anti-cancer treatment, and plays a pivotal role in breast cancer and lung cancer. The treatment of endometrial carcinoma is always delayed due to misdiagnosis for gynecological inflammation. In addition, it remains unclear how HMR1275 (flavopiridol) attenuates lesion of endometrial carcinoma. Our study was focused on the exploration of molecular mechanism underlying anti-cancer effect of HMR1275 (flavopiridol) via Livin. Endometrial carcinoma cell line Ishikawa was treated with HMR1275 (1 mu mol/L). MTT assay and flow cytometry examination were performed to assess the cell growth, proliferation and apoptosis of Ishikawa cells. Western blot was performed to examine the protein expression of Livin. siRNA was used for HMR1275 (1 mu mol/L) treated Ishikawa cells to inhibit the expression of Livin, and apoptosis was also examined by MTT assay and flow cytometry. HMR1275 (1 mu mol/L) treatment significantly reduced the growth rate of ishikawa cells, resulted in plasma membrane translocation of phosphatidylserine and activation of caspase. Protein expression of Livin was remarkably decreased after HMR1275 (1 mu mol/L) treatment. Moreover, down-regulation of Livin further enhanced apoptosis of ishikawa cells after HMR1275 (1 mu mol/L) treatment. Down-regulation of anti-apoptosis protein Livin promotes HMR1275 (flavopiridol)-induced apoptosis, and HMR1275 was possible to alleviate cancer via decreasing the expression of Livin.