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Background KLF5 plays a crucial role in stem cells of colorectum in cooperation with  Lgr5  gene. In this study, we aimed to explicate a regulatory mechanism of the  KLF5  gene product from a view of three-dimensional genome structure in colorectal cancer (CRC). Methods In vitro engineered DNA-binding molecule-mediated chromatin immunoprecipitation (enChIP)-seq method was used to identify the regions that bind to the  KLF5  promoter. Results We revealed that the  KLF5  promoter region interacted with the  KLF5  enhancer region as well as the transcription start site (TSS) region of the  Colon Cancer Associated Transcript 1 (CCAT1)  gene. Notably, the heterodeletion mutants of  KLF5  enhancer impaired the cancer stem-like properties of CRC cells. The KLF5 protein participated in the core-regulatory circuitry together with co-factors (BRD4, MED1, and RAD21), which constructs the three-dimensional genome structures consisting of  KLF5  promoter, enhancer and  CCAT1  TSS region. In vitro analysis indicated that KLF5 regulated  CCAT1  expression and we found that  CCAT1  expression was highly correlated with KLF5 expression in CRC clinical samples. Conclusions Our data propose the mechanistic insight that the KLF5 protein constructs the core-regulatory circuitry with co-factors in the three-dimensional genome structure and coordinately regulates  KLF5  and  CCAT1  expression in CRC.

A stem cell marker KLF5 regulates CCAT1 via three-dimensional genome structure in colorectal cancer cells