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The Klf6 gene, which belongs to Krüppel-like family of C2H2 zinc finger transcription factors, is greatly related to tumorigenesis via a high rate of somatic mutation in the carcinomas of prostate, liver, colon, stomach, lung, neck, pituitary, and nervous system: Furthermore, the pathways regulating the expressions of Klf6 splice variants termed Klf6-SV1, -SV2, and -SV3 remain obscure although their functional outcomes have been clear. In this study, the functional roles of Klf6 variants in the inhibition of cell proliferation induced by the disruption of Klf6-related super enhancer in human hepatoma (HepG2) cells were evaluated. As a result, the disruption of Klf6-related super enhancer not only induced the upregulation of Klf6-SV2 but also led to a significant reduction of proliferation in HepG2 cells. In addition, the disruption of Klf6-related super enhancer led to the induction of p21 and Bax genes mediated by the upregulation of Klf6-SV2. In conclusion, it was demonstrated that Klf6-related super enhancer modulates cell proliferation via the regulation of Klf6-SV2 expression in human hepatoma (HepG2) cells. The results provide the functional significance of Klf6-related super enhancer in understanding the transcriptional regulation mechanism of Klf6.

The Klf6-related super enhancer regulates Klf6-SV2 expression mediated proliferation in human hepatoma (HepG2) cells