Mitomycin C, a kind of antibiotic isolated from Streptomyces caespitosus or Streptomyces lavendulae, inhibits DNA synthesis through covalent mitomycin C-DNA adduct with EC50 values of 0.14μM in PC3 cells. Therefore, it was served as a chemotherapeutic agent that has demonstrated its antitumor activity and has been used widely in treatment of various cancers. [1]

Mitomycin-C enhanced TRAIL (TNF-related apoptosis-inducing ligand)-induced apoptosis in p53 deficient colon cancer HCT116 cells. In the cell viability assay, pretreated with 5M with mitomycin C for 24h and then exposure to 25ng/ml TRAIL  and 5μM mitomycin C for 12h in HCT116 cells showed surprisingly decreased cell viability. In the crystal violet staining assay showed 5μM mitomycin C combinated 25ng/ml TRAIL can substantially enhanced suppression effects of HCT116 cells. Pretreatment with 5μM mitomycin C can enhanced TRAIL initiated processing of caspase-8, -9, -3 and cleavage of RARP (poly-ADP-ribose polymerase, substrate of caspase-3).  The western blot assay showed in both HCT116 and HT29 cells, mitomycin C suppressed the expression anti apoptotic proteins Mcl-1, Bcl-2, Bcl-XL, and downregulated caspase-inhibitor c-IAP-1, XIAP, while upregulated expression of pro-apoptotic proteins Bax and Bim .[2]

The NMRI-Fox1nu nude mice was inoculated subcutaneously and then randomized to several groups: treated with electrochemotherapy and administrated 5mM mitomycin C or electrochemotherapy only or 5mM mitomycin C only. Results showed that tumor volume reduced in electrochemotherapy plus mitomycin C group, and mice survival rates were greater in electrochemotherapy plus mitomycin C group and mitomycin C group only, compared controls(p＜0.001). The tumor response rate was 53% for mitomycin C alone.[3]