Fig. 5: FOSL2 upregulated SEMA3C and c-Myc in HCT15-FR cells via the canonical Wnt–β-catenin signaling pathway. | Experimental & Molecular Medicine

Fig. 5: FOSL2 upregulated SEMA3C and c-Myc in HCT15-FR cells via the canonical Wnt–β-catenin signaling pathway.

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. 5

a Colocalization of FOSL2 and KLF6 in the nucleus of HCT15-FR cells by immunofluorescence. b Co-IP revealed no interaction between FOSL2 and KLF6. c TCF1 and c-Myc were upregulated in HCT15-FR cells, as shown by western blotting. d TCF1 and c-Myc decreased as SEMA3C was knocked down in HCT15-FR cells, as shown by western blotting. e β-Catenin markedly decreased in the nucleus following SEMA3C knockdown in HCT15-FR cells, as shown by western blotting. f Rac1–GTP was reduced in HCT15-FR cells when SEMA3C was knocked down, as shown by a Rac1–GTP pulldown assay. g FOSL2 expression was reduced in the nucleus in HCT15-FR cells with SEMA3C knockdown. h FOSL2 was upregulated as Wnt–β-catenin was activated by Wnt3a-CM. TCF1 was not influenced by β-catenin. i H3K23su, FOSL2, KLF6, SEMA3C, TCF1 and c-Myc expression levels increased as HDAC was suppressed.

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