Hydroxystilbenes and methoxystilbenes activate human aryl hydrocarbon receptor and induce CYP1A genes in human hepatoma cells and human hepatocytes

2017 ◽  
Vol 103 ◽  
pp. 122-132 ◽  
Author(s):  
Barbora Pastorková ◽  
Aneta Vrzalová ◽  
Petr Bachleda ◽  
Zdeněk Dvořák
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Hepatoma Cells ◽  
Human Hepatocytes ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Aryl Hydrocarbon

Different responses of primary normal human hepatocytes and human hepatoma cells toward cyanobacterial hepatotoxin microcystin-LR

Toxicon ◽  
2015 ◽  
Vol 105 ◽  
pp. 4-9 ◽  
Author(s):  
Tsuyoshi Ikehara ◽  
Junichi Nakashima ◽  
Shihoko Nakashima ◽  
Takeshi Yasumoto
Keyword(s):  
Hepatoma Cells ◽  
Human Hepatocytes ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Normal Human

EFFECT OF ARYL HYDROCARBON RECEPTOR AGONISTS AND LIPOPOLYSACCHARIDE ON BENZO(A)PYRENE GENOTOXICITY MARKERS

2019 ◽  
pp. 19-25 ◽  
Author(s):  
V. N. Babakov ◽  
N. Yu. Rogovskaya ◽  
I. D. Kurdyukov ◽  
P. P. Beltyukov ◽  
S. A. Dulov ◽  
...  
Keyword(s):  
Dna Repair ◽  
Aryl Hydrocarbon Receptor ◽  
P53 Protein ◽  
Control Level ◽  
Repair System ◽  
Human Hepatoma Cells ◽  
Kinase Activation ◽  
Receptor Agonists ◽  
Checkpoint Kinases ◽  
Aryl Hydrocarbon

The effect of aryl hydrocarbon receptor agonists (FICZ and ITE), as well as lipopolysaccharide under the toxic action of benzo(a)pyrene in HepaRG human hepatoma cells was evaluated. Active forms of the key stress-activated kinase cascades and DNA repair system proteins were used as markers of the genotoxic action of benzo(a)pyrene. A mixture of lipopolysaccharide with benzo(a)pyrene increases benzo(a)pyrene cytotoxicity and reduces the activation of DNA repair system proteins below the control level. Aryl hydrocarbon receptor agonists (FICZ and ITE) exhibit a cytoprotective effect against benzo(a) pyrene, enhance Akt1 kinase activation, and downregulate activation of the p53 protein and Chk1 and Chk2 checkpoint kinases. Thus, FICZ and ITE reduce the genotoxicity of benzo(a)pyrene.

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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