scholarly journals Small antisense RNA to cyclin D1 generated by pre-tRNA splicing inhibits growth of human hepatoma cells

FEBS Letters ◽  
2004 ◽  
Vol 576 (3) ◽  
pp. 481-486 ◽  
Author(s):  
Dazhi Lai ◽  
Shaojie Weng ◽  
Cui'e Wang ◽  
Lianquan Qi ◽  
Changming Yu ◽  
...  
Keyword(s):  
Cyclin D1 ◽  
Antisense Rna ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Trna Splicing

Inducible antisense RNA targeting amino acid transporter ATB0/ASCT2 elicits apoptosis in human hepatoma cells

2004 ◽  
Vol 286 (3) ◽  
pp. G467-G478 ◽  
Author(s):  
Bryan C. Fuchs ◽  
J. Christian Perez ◽  
Julie E. Suetterlin ◽  
Sofia B. Chaudhry ◽  
Barrie P. Bode
Keyword(s):  
Amino Acid ◽  
Antisense Rna ◽  
Amino Acid Transporter ◽  
Hepatoma Cells ◽  
Parp Cleavage ◽  
Rna Expression ◽  
Mrna Levels ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Acid Transporter

Amino acid transporter B0/ASC transporter 2 (ATB0/ASCT2) is responsible for most glutamine uptake in human hepatoma cells. Because this transporter is not expressed in normal hepatocytes, we hypothesized that its expression is necessary for growth of human liver cancer cells. To test this hypothesis, Sloan Kettering hepatoma (SK-Hep) cells were stably transfected with an inducible 1.3-kb ATB0/ASCT2 antisense RNA expression plasmid under the transcriptional control of mifepristone, a synthetic steroid. Induced antisense RNA expression in monolayer cultures decreased ATB0/ASCT2 mRNA levels by 73% and glutamine transport rates by 65% compared with controls after 24 h, leading to a 98% decrease in cell number after 48 h. Cellular death was attributable to apoptosis based on cellular blebbing, caspase-3 activation, vital dye and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining, and poly-(ADP-ribose) polymerase (PARP) cleavage. Transporter knockdown also markedly increased activities of caspases-2 and -9, marginally enhanced caspase-8 activity, and dramatically increased ASCT1 mRNA levels, presumably as a futile compensatory response. Apoptosis elicited via transporter silencing was not attributable to the double-stranded RNA-dependent protein kinase R (PKR) pathway. For comparison, glutamine deprivation also caused apoptotic cell death but with slower temporal kinetics, stimulated caspases-2 and -3 but not caspases-8 or -9 activities, and led to considerable PARP cleavage. Thus ASCT2 suppression exerts proapoptotic effects transcending those of glutamine starvation alone. We conclude that ATB0/ASCT2 expression is necessary for SK-Hep cell growth and viability and suggest that it be further explored as a selective target for human hepatocellular carcinoma.

scholarly journals Berberine Suppresses Cyclin D1 Expression through Proteasomal Degradation in Human Hepatoma Cells

2016 ◽  
Vol 17 (11) ◽  
pp. 1899 ◽  
Author(s):  
Ning Wang ◽  
Xuanbin Wang ◽  
Hor-Yue Tan ◽  
Sha Li ◽  
Chi Tsang ◽  
...  
Keyword(s):  
Cyclin D1 ◽  
Proteasomal Degradation ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
Human Hepatoma Cells

Rapid Downregulation of Cyclin D1 Induced by Geranylgeranoic Acid in Human Hepatoma Cells

2012 ◽  
Vol 64 (3) ◽  
pp. 473-480 ◽  
Author(s):  
Shohei Shimonishi ◽  
Takashi Muraguchi ◽  
Maiko Mitake ◽  
Chiharu Sakane ◽  
Kyoko Okamoto ◽  
...  
Keyword(s):  
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.

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