In a previous study, we elucidated the apoptotic mechanism mediated via Fas/FasL-dependent pathway in
mitomycin C-treated cervical
carcinoma cells. In this study, 2-D and MALDI-TOF analyses were performed in order to search
mitomycin C-induced modulators in cervical
carcinoma cells. Some
protein spots down- or up-regulated by
mitomycin C were separately selected from the 2-D
gels. Twenty
protein spots were identified from the 2-D
gels. Among the 20 spots, 11 spots were down-regulated, whereas 9 spots were up-regulated in SiHa/pRSV-luc cells by
mitomycin C. Three spots have not been identified in the database. Ku70-binding
protein (KUB3), MHC
class I antigen, MHC class I chain-related
protein A or multi-PDZ domain
protein 1, MAGUK P55 subfamily member 3 or lamda/iota
protein kinase C-interacting
protein, and GL014 or Sad1/unc-84
protein-like 1 were suppressed by
mitomycin C treatment. Heat shock 60 kDa
protein 1 (
chaperonin), similar to
heat shock protein 90 kDa
protein alpha or nine in centrosomal
protein isoform C,
NADP-dependent malic
enzyme, mitochondrial precursor,
GRB10 adaptor protein,
glycogenin-interacting
protein 1,
cystathionine gamma-lyase, G2/mitotic-specific
cyclin B2 or heat shock 90 kDa
protein 1 alpha,
peptidyl-prolyl cis-trans isomerase B, and PARP-2 (fragment) were induced by
mitomycin C. KUB3, Brca1, and E6 gene expressions were down-regulated by
mitomycin C in HPV-positive
cervical cancer cells, SiHa/pRSV-luc and SiHa. In these studies, we suggest that MMC down-regulated the expression levels of the upstream molecules of
DNA-double strand break repair system, non-homologous end joining or homologous recombination, resulting in the suppression of
cervical cancer cell growth.