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.
Methods:
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.
Tetracycline Derivative Minocycline Inhibits Autophagy and Inflammation in Concanavalin-A-Activated Human Hepatoma Cells
