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Hepatitis B virus X protein mediated suppression of miRNA-122 expression enhances hepatoblastoma cell proliferation through cyclin G1-p53 axis

Overview of attention for article published in Infectious Agents and Cancer, August 2016
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Title
Hepatitis B virus X protein mediated suppression of miRNA-122 expression enhances hepatoblastoma cell proliferation through cyclin G1-p53 axis
Published in
Infectious Agents and Cancer, August 2016
DOI 10.1186/s13027-016-0085-6
Pubmed ID
Authors

Manikankana Bandopadhyay, Neelakshi Sarkar, Sibnarayan Datta, Dipanwita Das, Ananya Pal, Rajesh Panigrahi, Arup Banerjee, Chinmay K. Panda, Chandrima Das, Shekhar Chakrabarti, Runu Chakravarty

Abstract

Hepatitis B virus (HBV) X protein (HBx) reported to be associated with pathogenesis of hepatocellular carcinoma (HCC) and miR-122 expression is down regulated in HCC. Previous studies reported miR-122 targets cyclin G1 (CCNG1) expression and this in turn abolishes p53-mediated inhibition of HBV replication. Here we investigated the involvement of HBx protein in the modulation of miR-122 expression in hepatoblastoma cells. Expression of miR-122 was measured in HepG2 cells transfected with HBx plasmid (HBx-HepG2), full length HBV genome (HBV-HepG2) and in constitutively HBV synthesizing HepG2.2.15 cells. CCNG1 mRNA (a direct target of miR-122) and protein expressions were also measured in both HBx-HepG2, HBV-HepG2 cells and in HepG2.2.15 cells. miR-122 expressions were analyzed in HBx-HepG2, HBV-HepG2 and in HepG2.2.15 cells after treatment with HBx mRNA specific siRNA. Expressions of p53 mRNA and protein which is negatively regulated by CCNG1 were analyzed in HBx transfected HepG2 cells; X silenced HBx-HepG2 cells and X silenced HepG2.2.15 cells. HBx induced cell proliferation in HepG2 cells was measured by cell proliferation assay. Flow cytometry was used to evaluate changes in cell cycle distribution. Expression of cell cycle markers were measured by real time PCR. Expression of miR-122 was down regulated in HBx-HepG2, HBV-HepG2 and also in HepG2.2.15 cell line compared to control HepG2 cells. CCNG1 expression was found to be up regulated in HBx-HepG2, HBV-HepG2 cells and in HepG2.2.15 cells. Following siRNA mediated silencing of HBx expression; increased miR-122 levels were documented in HBx-HepG2, HBV-HepG2 and in HepG2.2.15 cells. HBx silencing in HBx-HepG2 and HepG2.2.15 cells also resulted in increased p53 expression. FACS analysis and assessment of expressions of cell cycle markers revealed HBx induced a release from G1/S arrest in HepG2 cells. Further, cell proliferation assay showed HBx promoted proliferation of HepG2 cell. Our study revealed that HBx induced down regulation of miR-122 expression that consequently increased CCNG1 expression. This subsequently caused cell proliferation and release from G1/S arrest in malignant hepatocytes. The study provides the potential to utilize the HBx-miR-122 interaction as a therapeutic target to limit the development of HBV related HCC.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 19 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
China 1 5%
Unknown 18 95%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 21%
Researcher 3 16%
Student > Master 3 16%
Unspecified 1 5%
Other 1 5%
Other 2 11%
Unknown 5 26%
Readers by discipline Count As %
Medicine and Dentistry 3 16%
Biochemistry, Genetics and Molecular Biology 3 16%
Agricultural and Biological Sciences 2 11%
Unspecified 1 5%
Immunology and Microbiology 1 5%
Other 2 11%
Unknown 7 37%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 17 August 2016.
All research outputs
#12,395,487
of 14,011,199 outputs
Outputs from Infectious Agents and Cancer
#244
of 304 outputs
Outputs of similar age
#222,644
of 264,479 outputs
Outputs of similar age from Infectious Agents and Cancer
#1
of 1 outputs
Altmetric has tracked 14,011,199 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 304 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.6. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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