-Sristi Raj Rai, Amity University Kolkata
Alcohol consumption is not always the cause of hepatocellular carcinoma (HCC). People who drink little or no amount of alcohol can also develop a symptomless condition named non-alcoholic fatty liver disease (NAFLD), resulting from excessive storage of fats in liver cells that are now common among the masses.
An investigation by gene co-expression test uncovered that voltage-dependent anion channel (VDAC1) is associated with malfunctioning of the energy production unit of cells. Qualitative proteomics along with phenotypic-association examination reveals the presence of a considerably high amount of VDAC1 in tumor tissues which could be instantly connected with NAFLD related traits. The possible mechanism that drives the progression of the silent disease into Hepatocellular Carcinoma was studied using an extensive multiple-omics approach in mice strains.
Systems Biology an interdisciplinary path employed by Yanping Zhu et al. to construct a larger picture by fitting in small puzzle pieces, deduced VDAC1 located on the outer mitochondrial membrane acting as an entry/exit portal for ions and molecules is linked with an essential component of inner membrane – cardiolipin (CL) present in a significant amount. Moreover, CL appears to have a composition shift generating distortion in the membrane property and VDAC1 also quenches mature specie CL and pumps up nascent CL species level.
SOURCE – Zhu Y, Zhang C, Xu F, et al. System biology analysis reveals the role of voltage-dependent anion channel (VDAC1) in mitochondrial dysfunction during non-alcoholic fatty liver disease (NAFLD) progression into hepatocellular carcinoma (HCC) [published online ahead of print, 2020 Sep 17]. Cancer Sci. 2020;10.1111/cas.14651. doi:http://10.1111/cas.14651
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