Photodynamic Therapy (PDT), a promising and approved therapeutics for neoplastic and vascular disease, could induce
expression of angiogenic and survival molecules including vascular endothelial growth factor, cyclooxygenase-2
(COX-2), and MCL-1. However, the precise effect of MCL-1 which is a member of the bcl-2 family on PDT is not well
characterized. The work described here was aimed at determining whether expression of MCL-1 could exhibit a side
effect on PDT. The results showed that expression of MCL-1 was increased prominently after Hela cells treated with
PDT. By using confocal fluorescence microscopy and cell viability assay, it was found that overexpression of MCL-1
could have a vital influence on Photofrin-PDT-mediated apoptosis. Moreover, further analyses indicated that MCL-1
delayed translocation of Bax and release of cytochrome c from mitochrondria, further leading to cause a delay in cell
apoptosis in Hela cells treated with PDT. The process was associated with MCL-1 interaction directly with Bax. In
conclusion, overexpression of MCL-1 plays an important part in efficiency of PDT killing tumor cells, in other words,
MCL-1 overexpression decreases PDT induced apoptosis through directly interacting with Bax. These results suggest
that targeting MCL-1 expression might be a highly effective therapeutic measure for promoting the tumoricidal
effectiveness of PDT.
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