Increased expression of N-acetylglucosaminyltransferase-V in human hepatoma cells by retinoic acid and 1α,25-dihydroxyvitamin D3

2004 ◽  
Vol 36 (11) ◽  
pp. 2307-2319
Author(s):  
Cheorl-Ho Kim
2010 ◽  
Vol 249 (3) ◽  
pp. 224-230 ◽  
Author(s):  
Guo-Dong Zhou ◽  
Molly Richardson ◽  
Inayat S. Fazili ◽  
Jianbo Wang ◽  
Kirby C. Donnelly ◽  
...  

2002 ◽  
Vol 36 ◽  
pp. 181-182
Author(s):  
Masahisa Jinushi ◽  
Tetsuo Takehara ◽  
Tomohide Tatsumi ◽  
Tatsuya Kanto ◽  
Takuya Miyagi ◽  
...  

PLoS ONE ◽  
2011 ◽  
Vol 6 (7) ◽  
pp. e22545 ◽  
Author(s):  
Caroline Chauvet ◽  
Amandine Vanhoutteghem ◽  
Christian Duhem ◽  
Gaëlle Saint-Auret ◽  
Brigitte Bois-Joyeux ◽  
...  

MicroRNA ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 64-69 ◽  
Author(s):  
KumChol Ri ◽  
Chol Kim ◽  
CholJin Pak ◽  
PhyongChol Ri ◽  
HyonChol Om

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.


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