A novel interaction of nucleophosmin with BCL2-associated X protein regulating death evasion and drug sensitivity in human hepatoma cells

Hepatology ◽  
2013 ◽  
Vol 57 (5) ◽  
pp. 1893-1905 ◽  
Author(s):  
Shao-Jung Lo ◽  
Li-Ching Fan ◽  
Yow-Fu Tsai ◽  
Kuo-Yang Lin ◽  
Hsiao-Ling Huang ◽  
...  
Keyword(s):  
Drug Sensitivity ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
X Protein ◽  
Human Hepatoma Cells

scholarly journals Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

Oncotarget ◽  
2016 ◽  
Vol 7 (31) ◽  
pp. 50117-50130 ◽  
Author(s):  
Na-Na Tao ◽  
Hong-Zhong Zhou ◽  
Hua Tang ◽  
Xue-Fei Cai ◽  
Wen-Lu Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Drug Sensitivity ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
Glutathione S Transferase ◽  
Sirtuin 3 ◽  
Human Hepatoma Cells ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway

scholarly journals Hepatitis B virus-X protein upregulates the expression of p21wafl/cipl and prolongs G1→S transition via a p53-independent pathway in human hepatoma cells

Oncogene ◽  
2000 ◽  
Vol 19 (30) ◽  
pp. 3384-3394 ◽  
Author(s):  
Ui Sun Park ◽  
Sook Kyung Park ◽  
Yoon Ik Lee ◽  
Jong Gu Park ◽  
Young Ik Lee
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
X Protein ◽  
Human Hepatoma Cells ◽  
B Virus

The KLF6 Super Enhancer Modulates Cell Proliferation via MiR-1301 in Human Hepatoma Cells

MicroRNA ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 64-69 ◽  
Author(s):  
KumChol Ri ◽  
Chol Kim ◽  
CholJin Pak ◽  
PhyongChol Ri ◽  
HyonChol Om
Keyword(s):  
Cell Proliferation ◽  
Cellular Proliferation ◽  
Hepatoma Cells ◽  
Regulation Mechanism ◽  
Dependent Manner ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Over Expression ◽  
Super Enhancer ◽  
Engineering Changes

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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