Preferential inhibition of DNA polymerases?,?, and? from Novikoff hepatoma cells by inhibitors of cell proliferation

1996 ◽  
Vol 122 (2) ◽  
pp. 78-94 ◽  
Author(s):  
Gabriele Fox ◽  
Odilia Popanda ◽  
Lutz Edler ◽  
Heinz Walter Thielmann
Keyword(s):  
Cell Proliferation ◽  
Dna Polymerases ◽  
Hepatoma Cells ◽  
Novikoff Hepatoma

Evidence for reduced copying fidelity of DNA polymerases α, δ, and ε from Novikoff hepatoma cells

1997 ◽  
Vol 123 (11-12) ◽  
pp. 659-668 ◽  
Author(s):  
Gabriele Fox ◽  
Odilia Popanda ◽  
H. W. Thielmann
Keyword(s):  
Dna Polymerases ◽  
Hepatoma Cells ◽  
Novikoff Hepatoma ◽  
Copying Fidelity

Purified DNA polymerases α, σ, and ε from the highly malignant Novikoff hepatoma cells have lowered copying fidelity

1995 ◽  
Vol 121 (S1) ◽  
pp. A16-A16
Author(s):  
G. Fox ◽  
O. Popanda ◽  
H. W. Thielmann
Keyword(s):  
Dna Polymerases ◽  
Hepatoma Cells ◽  
Novikoff Hepatoma ◽  
Copying Fidelity

HAb18G/CD147 enhances cell proliferation by promoting G0/G1 to S transition by ERK1/2 dependent cyclin D1 synthesis in human hepatoma cells

2010 ◽  
Vol 34 (8) ◽  
pp. S45-S45
Author(s):  
Yunshan Guo ◽  
Juan Tang ◽  
Zhinan Chenand Jianli Jiang
Keyword(s):  
Cell Proliferation ◽  
Cyclin D1 ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
Human Hepatoma Cells

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.

Phenobarbital inhibits calpain activity and expression in mouse hepatoma cells

2016 ◽  
Vol 397 (1) ◽  
pp. 91-96 ◽  
Author(s):  
Nicola Groll ◽  
Ferdinand Kollotzek ◽  
Jens Goepfert ◽  
Thomas O. Joos ◽  
Michael Schwarz ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Transcriptional Regulation ◽  
Antiepileptic Drug ◽  
Signaling Pathway ◽  
Constitutive Androstane Receptor ◽  
Hepatoma Cells ◽  
Liver Cells ◽  
Mrna Levels ◽  
Calpain Activity ◽  
Mouse Hepatoma

Abstract The antiepileptic drug phenobarbital (PB) exerts hepatic effects related to cell proliferation and tumorigenesis which are closely linked to the Wnt/β-catenin signaling pathway. This pathway is, amongst others, regulated by calpain proteases. We now identified PB as an inhibitor of Wnt/β-catenin signaling in mouse hepatoma cells. Further analyses revealed that PB inhibits calpain activity, an effect which is at least in parts mediated by a transcriptional regulation of calpain mRNA levels and which is furthermore independent of the constitutive androstane receptor, the known mediator of most effects of PB in liver cells.

Initiation of transcription in permeabilized novikoff hepatoma cells

1980 ◽  
Vol 4 (2) ◽  
pp. 175-184 ◽  
Author(s):  
B SAMAL ◽  
N BALLAL ◽  
H BUSCH
Keyword(s):  
Hepatoma Cells ◽  
Novikoff Hepatoma ◽  
Initiation Of Transcription
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