Fig. 8: FOSL2 or KLF6 knockdown induced a decrease in 5-FU resistance, which could be rescued by SEMA3C overexpression. | Experimental & Molecular Medicine

Fig. 8: FOSL2 or KLF6 knockdown induced a decrease in 5-FU resistance, which could be rescued by SEMA3C overexpression.

From: KLF6-mediated recruitment of the p300 complex enhances H3K23su and cooperatively upregulates SEMA3C with FOSL2 to drive 5-FU resistance in colon cancer cells

Fig. 8

a FOSL2 knockdown downregulated the 5-FU-resistance-promoting proteins SEMA3C, β-catenin, TCF1 and c-Myc. When SEMA3C was overexpressed, this downregulation was impaired. b The decrease in 5-FU resistance induced by FOSL2 knockdown in a nude mouse subcutaneous tumor model could be rescued by SEMA3C overexpression. The tumor volume was measured every 4 days after injection. The tumor weights of the subcutaneous xenografts are shown. c Colony formation assays indicated that SEMA3C overexpression reversed the FOSL2-knockdown-induced decrease in 5-FU resistance in HCT15-FR cells. d KLF6 knockdown downregulated the 5-FU-resistance-promoting proteins SEMA3C, β-catenin, TCF1 and c-Myc. This downregulation was impaired by SEMA3C overexpression. e EdU assays revealed that SEMA3C overexpression rescued the decrease in 5-FU resistance in HCT15-FR cells induced by KLF6 knockdown. f Colony formation assays suggested that SEMA3C overexpression reversed the KLF6-knockdown-induced decrease in 5-FU resistance in HCT15-FR cells. g The 5-FU-resistance-promoting proteins KLF6, H3K23su, SEMA3C and c-Myc were upregulated by TSA (10 µM). This upregulation could be reversed by KLF6 knockdown. h SEMA3C knockdown downregulated the expression of the 5-FU-resistance-promoting proteins β-catenin and c-Myc. When β-catenin was overexpressed, this downregulation was impaired. i β-Catenin overexpression impaired the SEMA3C-knockdown-induced increase in apoptosis rates in HCT15-FR cells.

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