Fig. 2. SGK2 silencing sensitizes ovarian cancer cells to platinum via a kinase-dependent mechanism.

a Schematic representation of SGK2 dominant negative (DN) (pLPC-SGK2^T193A/S356A) and constitutively active (CA) (pLPC-SGK2^S356D) constructs (upper panel). Overexpression of the different SGK2 constructs in TOV21G cells was confirmed by WB (lower panel). Vinculin was used as loading control. b Graph reporting cell viability of TOV21G cells described in a and treated with increasing doses of CBDCA. Results are expressed as survival ratio (%) of CBDCA treated over untreated cells (set as 100% as reference) (e.v = empty vector). c Graph reporting cell viability of MDAH cells treated with the indicated doses of GSK650394 (GSK), followed by CBDCA 140 μg/ml as depicted in the experimental timeline shown above the graph. d Graph reporting cell viability of MDAH cells treated for 36 h with GSK 35 μM, in the presence of CBDCA 140 μg/ml for the last 16 h as depicted in the shown experimental timeline. e Graphs reporting cell viability of SGK2-expressing (TOV21G, OV90, and SKOV3) and SGK2 not-expressing cell lines (HuNoEOC, COV318, TOV112D) treated with GSK 35 μM, CBDCA at the indicated doses used alone or in combination using the timeline reported in d. Data represent the mean ± SD of three independent experiments. Significance was calculated using two-tailed, unpaired Student’s t test. ****p < 0.0001, ***p < 0.001, **p < 0.01, ns not significant. (See also Fig. S3).