fig3

KLF5 promotes tumor proliferation and oxaliplatin resistance via chromatin remodeling in KRAS-mutated colorectal cancer

Figure 3. KLF5 promotes chromatin accessibility in KRAS-mutant CRC cells. (A and B) CUT&Tag sequencing analysis of control (SHNC) and KLF5-knockdown groups (SHKLF5). Signal distribution is calculated across TSSs, TESs, and flanking ± 3 kb regions, with corresponding heatmaps; (C) Pie chart summarizing the distribution of peaks across functional regions; (D) Venn diagram comparing differential peak-associated genes (SHKLF5 vs. SHNC) and RNA-seq-derived differentially expressed genes, identifying 1,400 overlapping genes; (E) GO pathway analysis of the overlapping genes; (F) KEGG pathway analysis of the overlapping genes. KLF5: Krüppel-like factor 5; CRC: colorectal cancer; CUT&Tag: cleavage under targets and tagmentation; SHNC: short hairpin negative control; SHKLF5: short hairpin KLF5; TSS: transcription start site; TES: transcription end site; GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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