Features | Partner Sites | Information | LinkXpress
Sign In
GLOBETECH PUBLISHING LLC
GLOBETECH MEDIA
GLOBETECH PUBLISHING LLC

Reversing Loss of miR-122 Helps Treat Liver Cancer

By BiotechDaily International staff writers
Posted on 01 Aug 2012
A study revealed that loss of the miR-122 molecule in liver cells might cause liver cancer and that restoring the molecule might slow tumor growth.

Liver cancer is the third leading cancer killer worldwide and new treatments are greatly needed. The animal study was led by researchers at the Ohio State University (OSU) Comprehensive Cancer Center-Arthur G. James Cancer Hospital (Columbus, USA) and OSU’s Richard J. Solove Research Institute (OSUCCC-James). The scientists examined what occurs when liver cells lack a molecule called microRNA-122 (miR-122). They found that when the molecule is missing, the liver develops fat deposits, inflammation, and tumors that resemble hepatocellular carcinoma (HCC), the most common form of liver cancer.

When the researchers synthetically restored miR-122 to nearly normal levels by delivering the miR-122 gene into liver cells, it considerably reduced the size and number of tumors, with tumors making up 8% on average of liver surface area in treated animals versus 40% in control animals.

The study was published July 23, 2012, in the Journal of Clinical Investigation. “These findings reveal that miR-122 has a critical tumor-suppressor role in the healthy liver, and they highlight the possible therapeutic value of miR-122 replacement for some patients with liver cancer,” said study leader Dr. Kalpana Ghoshal, associate professor of pathology and a member of the OSUCCC-James Experimental Therapeutics Program.

MiR-122 is found principally in liver cells--it is the most plentiful microRNA in those cells--and it plays a major role in regulating cholesterol in the body. This microRNA is lost in some people with HCC, however, resulting in a poor prognosis.

For this study, Dr. Ghoshal and her colleagues developed a strain of mice that lacks miR-122 and develops HCC through the progression of events that begins with fatty liver deposits followed by inflammation and liver cancer. The researchers then used a second strain of mice that spontaneously develops liver cancer due to overexpression of a cancer-causing gene called MYC. The researchers delivered miR-122 into the animals’ livers during tumor development. Three weeks later, those treated with the molecule had smaller and fewer tumors. “The model we developed for these studies will not only facilitate our understanding of liver biology, but it will also be good for testing therapeutic efficacy of newly developed drugs against liver disease, including HCC,” Dr. Ghoshal stated.

Dr. Ghoshal also noted that research by other scientists has shown that Hepatitis C virus requires miR-122 for replication. “Because our findings demonstrate what happens when miR-122 is lost in liver cells, they might help improve the safety of new drugs that treat Hepatitis C virus infection by blocking miR-122,” she concluded.

Related Links:

Ohio State University Comprehensive Cancer Center-Arthur G. James Cancer Hospital



Channels

Genomics/Proteomics

view channel
Image: Cancer cells, left, were pretreated with a drug that blocks the ERK signal, and right, without the pretreatment. Top cells are untreated, while the bottom ones are stimulated (Photo courtesy of the Weizmann Institute of Science).

Prevention of ERK Nuclear Translocation Blocks Cancer Proliferation in Animal Models

A team of cell biologists has shown that the cancer promoting effects of ERK dysregulation can be blocked by low molecular weight drugs that prevent translocation of this kinase from the cells' cytoplasm... Read more

Drug Discovery

view channel
Image: Star-like glial cells in red surround alpha-beta plaques in the cortex of a mouse with a model of Alzheimer\'s disease (Photo courtesy of Strittmatter laboratory/Yale University).

Experimental Cancer Drug Reverses Symptoms in Mouse Model of Alzheimer's Disease

An experimental, but clinically disappointing drug for treatment of cancer has been found to be extremely effective in reversing the symptoms of Alzheimer's disease (AD) in a mouse model.... Read more

Biochemistry

view channel
Image:  Model depiction of a novel cellular mechanism by which regulation of cryptochromes Cry1 and Cry2 enables coordination of a protective transcriptional response to DNA damage caused by genotoxic stress (Photo courtesy of the journal eLife, March 2015, Papp SJ, Huber AL, et al.).

Two Proteins Critical for Circadian Cycles Protect Cells from Mutations

Scientists have discovered that two proteins critical for maintaining healthy day-night cycles also have an unexpected role in DNA repair and protecting cells against genetic mutations that could lead... Read more

Business

view channel

NanoString and MD Anderson Collaborate on Development of Novel Multi-Omic Expression Profiling Assays for Cancer

The University of Texas MD Anderson Cancer Center (Houston, TX, USA) and NanoString Technologies, Inc. (Seattle, WA, USA) will partner on development of a revolutionary new type of assay—simultaneously profiling gene and protein expression, initially aiming to discover and validate biomarker signatures for immuno-oncology... Read more
 

Events

21 Apr 2015 - 23 Apr 2015
21 Apr 2015 - 23 Apr 2015
Copyright © 2000-2015 Globetech Media. All rights reserved.