Fig. 1: Knocking down MECOM in SKOV3 and OVSAHO ovarian cancer cells harboring MECOM amplification results in proliferation and migration defect. | Cell Death Discovery

Fig. 1: Knocking down MECOM in SKOV3 and OVSAHO ovarian cancer cells harboring MECOM amplification results in proliferation and migration defect.

From: Epigenetic targeting of MECOM/KRAS axis by JIB-04 impairs tumorigenesis and cisplatin resistance in MECOM-amplified ovarian cancer

Fig. 1

A High MECOM expression was observed in ovarian cancer patient samples (Tumor; n = 12) when compared to ovarian surface epithelium tissue samples (Normal; n = 12) (p value < 0.0001) B Tumor tissues of high grade serous ovarian carcinoma patients (HGSOC; n = 53) express high MECOM compared to normal ovarian surface epithelium tissues (Normal; n = 10) (p value < 0.001). C Selection of cell lines OVSAHO and SKOV3 with MECOM amplification, and non-amplified cell A2780 for the study based on Cancer Cell Line Encyclopedia (CCLE) dataset. D, E, F Western blotting demonstrated high protein expression of MECOM (MDS1-EVI1) and EVI1 in OVSAHO and SKOV3 ovarian cancer cells in comparison to A2780 non-amplified cells. Bar graphs provide quantification of protein bands analysed by densitometric analysis. G, H Western blotting and densitometric analysis confirmed efficient knockdown of MECOM in both SKOV3 and OVSAHO cells. siRNA targeting luciferase (siLuc) served as control. I Colony forming assay demonstrated proliferation defect in both cell lines upon MECOM silencing. J MECOM silencing reduced phosphorylation of ERK1/2 in SKOV3 cells. Bar graph provides the quantification of densitometric analysis of protein bands. K Transwell migration assay showed defective migratory potential of MECOM deficient cells L RT-qPCR analysis for ZEB1, Vimentin, and N-cadherin in SKOV3 cells upon MECOM silencing. Uncropped western blot images corresponding to Fig. 1G, H, and J were shown in Supplementary information.

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