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. 2021 Oct 30;41(2):191–203. doi: 10.1038/s41388-021-02077-w

Fig. 3. GRB7 is sufficient for MEKi resistance in KRAS mutation colon cancer cells.

Fig. 3

A Clonogenic assay showing that knockdown of GRB7 with shRNAs enhanced response to MEKi. B Short-term survival curves identifying that knockdown of GRB7 increased the sensitivity of MEKi. Results are shown relative to DMSO-treated controls (mean ± SD, n = 5; dashed line, 50% inhibition). C–F Knockdown of GRB7 significantly induced apoptosis upon AZD6244 treatment in HCTT16 (C, D) and SW480 (E, F). Cells were treated with AZD6244 for 48 h (HCT116) or 24 h (SW480). Data represented as mean ± SD (n = 3). G–I Clonogenic assay showing that GRB7 overexpression conferred resistance to AZD6244. (H) Quantification of HCT116, (I) Quantification of SW480. Data represented as mean ± SD (n = 3). J, K Induction of anti-apoptosis upon overexpression of GRB7 in HCT116. K Quantification of (J). Data represented as mean ± SD (n = 3). *p < 0.05, **p < 0.01, ***p < 0.001, or ****p < 0.0001.