Fig. 4: KLF6 cooperated with FOSL2 to regulate SEMA3C expression. | Experimental & Molecular Medicine

Fig. 4: KLF6 cooperated with FOSL2 to regulate SEMA3C expression.

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. 4

a PPI network illustrating DETFs associated with H3K23su DERs. The network nodes indicate proteins, and the colored edges represent evidence of different types of PPIs. Strong relationships and networks are indicated by solid lines and were clustered using the Markov algorithm with the default settings. b Coexpression of DETFs associated with H3K23su DERs in Homo sapiens identified using STRING. c H3K23su, FOSL2 and KLF6 expression levels in HCT15-FR cells were greater than those in HCT15-Pa cells, as determined by western blotting. d ChIP–qPCR confirmed that the SEMA3C promoter was enriched in the FOSL2 binding site. e SEMA3C expression was greater in HCT15-FR cells than in HCT15-Pa cells. f Expression levels of KLF6, FOSL2 and SEMA3C in the NC (negative control), FOSL2-knockdown, KLF6-knockdown, and FOSL2- and KLF6-knockdown groups of HCT15-FR cells. SEMA3C expression decreased with FOSL2 or KLF6 knockdown. The decrease in SEMA3C expression was more marked when FOSL2 and KLF6 were knocked down together. g Protein levels of FOSL2, KLF6 and SEMA3C in the NC, FOSL2-overexpression, KLF6-overexpression, and FOSL2- and KLF6-overexpression groups of HCT15-Pa cells. SEMA3C expression increased as FOSL2 or KLF6 overexpression increased, and the increase in SEMA3C expression was more marked when FOSL2 and KLF6 were overexpressed together in HCT15-Pa cells. h FOSL2 and KLF6 were highly enriched near the TSS. i Intensive colocalization relationship between KLF6 and FOSL2. j KLF6 knockout impaired FOSL2 and H3K23su binding to the promoter of SEMA3C.

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