The proportion of apoptotic cells was considerably induced in co treated cells in comparison to apicidin alone treated cells. These results claim that inhibition of apicidininduced autophagy (-)-MK 801 increased the induction of apoptosis by apicidin. Apicidin is a novel cyclic tetrapeptide with an extensive spectrum of anti proliferative activity against a variety of cancer cell lines. In this study, the anti tumor efficacy of apicidin was evaluated against YD 8 and YD 10B human OSCC cells. On the inhibition of apoptosis and cell proliferation we first have examined the results of apicidin. Our data indicated that apicidin dramatically induced cell cycle arrest at G2/M periods, which is mediated by inducing the levels of p21WAF1 and lowering the levels of cyclin B1, r cdc2 and p53. These email address details are similar to a previous study which showed that treatment of SK OV 3 human ovarian carcinoma cells with apicidin caused a growth in the proportion of cells in the G2/M cycle. Though there was the same effect of apicidin caused G2/M cycle charge, the p53 status in the cells was different. Our results suggest that apicidin may contributes to G2/M charge Urogenital pelvic malignancy by induction of p21WAF1 in a p53 independent way. HDAC inhibitors find a way to alter the expression of apoptotic proteins and induce cyst cell death with the biochemical and morphological traits of apoptosis. It was previously shown apicidin induces apoptosis in human endometrial cancer cells through the launch of mitochondrial cytochrome C and activation of caspases. Consistent with these findings, today’s study indicated that apicidin treatment contributes to the release of cytochrome C to the cytosol and activation of caspase 9, 7 and 3, which was confirmed by PARP bosom in OSCC cells. Autophagy is induced in cancer cells as a process of stress tolerance when cells are subjected to nutrient deprivation, hypoxia, reactive oxygen species or anticancer treatments. There are many stories of HDAC inhibitor induced autophagy. Valproic acid triggered autophagy and destabilizes Sae2 in yeasts. Suberoylanilide hydroxamic acid mediated autophagy in addition to apoptosis in HeLa cells. FK228 mediated autophagy in rhabdomyosarcoma cells. We next examined whether autophagy is induced by apicidin, which has been shown to Bazedoxifene dissolve solubility trigger apoptotic cell death in human OSCC. After autophagy is set up by ATGs, LC3 is converted to the active LC3 II type, which is inserted in to the double membrane of autophagophores and autophagosomes. The results show that apicidin caused autophagy, which was characterized by the increased levels of LC3 II and ATG5, the accumulation of AVOs. To our knowledge, this is actually the first study to show that apicidin triggers autophagy in OSCC cells.