MicroRNA-122 mimic transfection contributes to apoptosis in HepG2 cells

Molecular Medicine Reports
Hongyan HuangShaoyang Li

Abstract

There is currently a requirement for effective treatment strategies for human hepatocellular carcinoma (HCC), a leading cause of cancer‑associated mortality. MicroRNA-122 (miR-122), a repressor of the endogenous apoptosis regulator Bcl‑w, is frequently downregulated in HCC. Thus, it is hypothesized that the activation of miR‑122 may induce selective hepatocellular apoptosis via caspase activation in a model of HCC. In the present study, an miR‑122 mimic transfection was performed in HepG2 cells, and used to investigate the role and therapeutic potential of miR‑122 in the regulation of HCC‑derived cell lines. The apoptotic rates of HepG2 cells were significantly increased following miR‑122 mimic transfection. Reverse transcription‑polymerase chain reaction analysis revealed that Bcl‑w mRNA was significantly reduced, while the mRNA levels of caspase‑9 and caspase‑3 were markedly increased. The immunocytochemistry results supported the mRNA trends. Collectively, the present results suggest that endogenous miR‑122 contributes to HepG2 apoptosis and that transfection of mimic miR‑122 normalizes apoptotic levels in a model of HCC.

References

Mar 9, 2000·Nature Cell Biology·J C MartinouB Antonsson
Jun 26, 2001·Cell Death and Differentiation·L A O'ReillyA Strasser
Feb 18, 2003·Transplantation·Satoshi KaiharaKoichi Tanaka
Mar 11, 2005·Best Practice & Research. Clinical Gastroenterology·Katherine A McGlynn, W Thomas London
Mar 12, 2005·CA: a Cancer Journal for Clinicians·D Max ParkinPaola Pisani
Aug 12, 2008·Biochemical and Biophysical Research Communications·Cliff Ji-Fan LinJen-Leih Wu
Feb 20, 2009·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Sean F AltekruseMarsha E Reichman
May 15, 2009·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Teng XuShi-Mei Zhuang
Nov 7, 2009·Scandinavian Journal of Gastroenterology·Xia WuZhaohua Zhong
Jun 10, 2010·Journal of the American Chemical Society·Douglas D YoungAlexander Deiters
Sep 13, 2012·Experimental and Therapeutic Medicine·Lei ShenLin Fang
Feb 18, 2014·Journal of Gastroenterology·Kazuhiko NakaoTatsuki Ichikawa

❮ Previous
Next ❯

Citations

Nov 26, 2019·Andrologia·Sara RahbarMarefat Ghaffari Novin
Dec 19, 2019·Cancer Metastasis Reviews·Karina Bezerra SalomãoMaría Sol Brassesco
Dec 15, 2020·Journal of Controlled Release : Official Journal of the Controlled Release Society·Hongzhi WangPeixuan Guo
Dec 11, 2020·BioMed Research International·Mohamed H YousefAnwar Abdelnaser
Apr 30, 2021·Saudi Journal of Biological Sciences·Mohamed A ElkadyMostafa M Elshafey

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis in Cancer

Apoptosis is an important mechanism in cancer. By evading apoptosis, tumors can continue to grow without regulation and metastasize systemically. Many therapies are evaluating the use of pro-apoptotic activation to eliminate cancer growth. Here is the latest research on apoptosis in cancer.

CREs: Gene & Cell Therapy

Gene and cell therapy advances have shown promising outcomes for several diseases. The role of cis-regulatory elements (CREs) is crucial in the design of gene therapy vectors. Here is the latest research on CREs in gene and cell therapy.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.