Involvement of Akt in mitomycin C and its analog triggered cytotoxicity in MCF-7 and K562 cancer cells.

ABSTRACT: Mitomycin C (MC) is a well-known DNA alkylating agent. MC analog, 10-decarbamoyl mitomycin C (DMC), unlike MC, has stronger effects on cancer with p53 mutation. We previously demonstrated that MC/DMC could activate p21^WAF1/CIP1 in MCF-7 (p53-proficient) and K562 (p53-deficient) cells in a p53-independent mode. This study aimed to elucidate the upstream signaling pathway of p21^WAF1/CIP1 activation triggered by MC/DMC. Besides p53, Akt plays an important role on deactivating p21^WAF1/CIP1 . The results showed that MC/DMC inhibited Akt in MCF-7 cells, but not in K562 cells. By knocking down p53, the Akt inhibition in MCF-7 cells was alleviated. This implied that t

SUBMITTER: Cheng SY 

PROVIDER: S-EPMC6251731 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature