MTT analysis of cell viability unveiled thatmitomycin D at concentrations ranging from10 to 60 g/ml, time dependently inhibited cell growth and caused the over expression of p53. Thereafterwe pre treated the cells with 3 MAand then denver incubated the cellswith silibinin andmitomycin C for 1-2 h. The growth inhibition of cells in each groupwasmeasured by MTT assay. As shown in Fig. 5C, mitomycin C induced mobile progress inhibition was suppressed by silibinin treatment, but, this was corrected by autophagy chemical 3 MA pre treatment. And the protein amounts of p53 and the proportion were respectively assessed byWestern blot Pemirolast concentration analysis and by flow cytometric analysis of PI staining. As shown in Fig. 5D, 3 MA pre therapy partly abrogated silibinins suppressive effect on p53 expression. More over, in the cells co treatedwith 3 MA, silibinin andmitomycin C, the proportion of cells in sub G0/1 section was increased compared to that of mitomycin and silibinin C co treated cells. For that reason, silibinininduced autophagy assisted cell survival in mitomycin C induced cell insult. ?The aforementioned results gave a clue that silibinin caused autophagy by controlling p53 degree, subsequently facilitating the expression of NF B. By comparison, our subsequent data showed that the connection between p53 and autophagy was active. Autophagy chemical 3 MA pre treatment generated the escalation of p53 stage and the fall Meristem of NF T and r NF T levels. Hence autophagy suppressed p53 expression, thereby augmenting the expression and the activation of NF B. Reviewing all of the aforementioned results,we drew a conclusion that reduction of p53 by silibinin treatment triggered NF B activation and therefore caused autophagy. P53 expression there’s a feedback loop between autophagy induction and p53 suppression, namely, p53 suppression evoked autophagy further accelerated silibinins suppressive effect. Furthermore, autophagy antagonized mitomycin C induced cell apoptosis. Owing to its great antiproliferative and anti apoptotic efficacies in bladder cancer, prostate cancer and breast cancer, silibinin is now a hot spot in cancer research. But, our previous studies have documented the anti apoptotic properties of silibinin in mitomycin and UVB C induced A375 S2 cell death models. And these effects are company related with silibinins anti p53 activity. angiogenesis research We offer these protective mechanisms are related to its suppressive effect on regulating p53 expression. Relative to this assumption, the current study has shown that inhibition of p53 evokes the occurrence of autophagy in A375 S2 cells, which is a potential mechanismthrough which cells avoid being killed by mitomycin C. Besides, inside our other research silibinin induced autophagy can also be determined in other cell lines such as in human fibrosarcoma HT1080 cell line and in human epidermoid carcinoma A431 cell line. And the corresponding autophagy induction systems are still under study.