Abstract
Nuclear protein phosphatase Wip1 regulate sensitivity of human colorectal cancer cells to DNA damaging anti-cancer agents
Highlights
Transfected cells were incubated in the presence or absence of HDACi sodium butyrate and afterwards, the efficiency of DNA repair was evaluated by measurement of the luciferase activity
We have shown that the recovery of DNA has occurred less efficiently in the presence of sodium butyrate in transformed cells, while in normal fibroblasts sodium butyrate did not affect the NHEJ-repair efficiency
We showed that overexpression of Wip1 led to phosphatase accumulation in the nucleus and affected DNA damage response in colorectal cancer cells by decreasing the sensitivity of DLD1 cells to combination anticancer drugs used in clinics for the treatment of colorectal cancer, oxaliplatin and 5-fluouracil
Summary
Methods: To model the NHEJ repair mechanism we used the host-cell reactivation assay. A luciferase reporter vector pGL3-luc was damaged with endonuclease and etoposide, and introduced into E1A+Ras-transformed and normal (NIH3T3) mouse fibroblasts, using lipofectamine transfection. Transfected cells were incubated in the presence or absence of HDACi sodium butyrate and afterwards, the efficiency of DNA repair was evaluated by measurement of the luciferase activity. We have shown that the recovery of DNA has occurred less efficiently in the presence of sodium butyrate in transformed cells, while in normal fibroblasts sodium butyrate did not affect the NHEJ-repair efficiency.
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