Fig. 3

pLCK is localized in nucleus in response to DNA damage and LCK disruption suppresses BRCA1 expression in response to DNA damage. A Western blot analysis of T-LCK, BRCA1 and yH2AX expression following 24 h etoposide or MMS treatment, followed by 24 h recovery in CP70 cells. B CP70 LCK OE cells were treated without or with etoposide, harvested and cytoplasmic and nuclear fractions isolated, followed by western blot analysis. C Immunofluorescence of pLCK in CP70 cells treated without or with etoposide. Scale bar represents 10 µm. (D) Human tissue samples of endometrioid ovarian cancer were processed for immunohistochemistry to detect LCK protein expression. Two representative images are shown, and the selected area is magnified. E CP70 cells were transduced with control shRNA (shCon) or LCK specific shRNA (KD1, KD2), treated with etoposide or without and BRCA1 expression detected by immunoblots. GAPDH served a loading control. F CP70 parental or LCK CRISPR KO were treated with etoposide or without and BRCA1 expression detected by immunoblots. GAPDH served a loading control. All experiments were replicated three times