Skip to main content
. Author manuscript; available in PMC: 2020 May 1.
Published in final edited form as: Cancer Res. 2019 Mar 15;79(9):2195–2207. doi: 10.1158/0008-5472.CAN-18-2133

Figure 1: Menin is upregulated in colon cancer and provides resistance to gefitinib.

Figure 1:

A) TCGA database analysis comparing menin expression in non-cancerous colonic epithelial samples compared to colon cancer samples. Log2-transformed, normalized counts are shown for menin, dividing the plot to separate normal and tumor samples. *** p = 3.31E-14. B) Menin IHC in colon cancer and adjacent normal colonic mucosa, with two representative examples shown, 100X magnification. C-D) HT-29 cells transduced with either scrambled or menin shRNAs (C), then cell growth was assessed after 96 hours by the MTS assay (D). E-F) HT-29 cells transduced with either vector or menin (E), then cell growth was assessed after 96 hours by the MTS assay (F). G) HT-29 cells transduced with either scrambled or menin shRNAs, then treated with varying concentrations of gefitinib. Cell growth was assessed after 96 hours by the MTS assay. H) HT-29 cells transduced with either lentiCRISPRv2 vector or menin sgRNA, then treated with varying concentrations of gefitinib. Cell growth was assessed after 96 hours by the MTS assay. I) HT-29 cells transduced with scrambled or menin shRNAs, then protein levels were assessed by western blot after 96 hours. 10 μM gefitinib. J) HT-29 cells transduced with either lentiCRISPRv2 vector or menin sgRNA, then protein levels were assessed by western blot after 96 hours. 10 μM gefitinib. * p < 0.05.