Background: Recent studies have attempted to elucidate the function of super enhancers
by means of microRNAs. Although the functional outcomes of miR-1301 have become clearer, the
pathways that regulate the expressions of miR-1301 remain unclear.
Objective: The objective of this paper was to consider the pathway regulating expression of miR-
1301 and miR-1301 signaling pathways with the inhibition of cell proliferation.
Method: In this study, we prepared the cell clones that the Klf6 super enhancer was deleted by means
of the CRISPR/Cas9 system-mediated genetic engineering. Changes in miR-1301 expression after
the deletion of the Klf6 super enhancer were evaluated by RT-PCR analysis, and the signal pathway
of miR-1301 with inhibition of the cell proliferation was examined using RNA interference technology.
Results: The results showed that miR-1301 expression was significantly increased after the deletion
of the Klf6 super enhancer. Over-expression of miR-1301 induced by deletion of the Klf6 super enhancer
also regulated the expression of p21 and p53 in human hepatoma cells. functional modeling of
findings using siRNA specific to miR-1301 showed that expression level changes had direct biological
effects on cellular proliferation in Human hepatoma cells. Furthermore, cellular proliferation assay
was shown to be directly associated with miR-1301 levels.
Conclusion: As a result, it was demonstrated that the over-expression of miR-1301 induced by the
disruption of the Klf6 super enhancer leads to a significant inhibition of proliferation in HepG2 cells.
Moreover, it was demonstrated that the Klf6 super enhancer regulates the cell-proliferative effects
which are mediated, at least in part, by the induction of p21and p53 in a p53-dependent manner. Our
results provide the functional significance of miR-1301 in understanding the transcriptional regulation
mechanism of the Klf6 super enhancer.