Dual behavior of HCV Core gene in regulation of apoptosis is important in progression of HCC

Saleem, Sidrah; Ashfaq, Usman Ali; Khaliq, Saba; Samreen, Baila; Afzal, Nadeem

doi:10.1016/j.meegid.2012.01.006

Cited by 35 publications

(27 citation statements)

References 35 publications

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“…In acute HCV infection, intensive hepatocyte apoptosis helps to eliminate the virus. In chronic HCV, hepatocyte apoptosis is accompanied by cell proliferation and ensures persistent infection, as observed in chronic HBV patients 60. An important difference is noted between HBV and HCV infection: HCV-induced apoptosis is not strongly correlated with the amount of virus but is rather immune-oriented 61.…”

Section: Hepatocyte Apoptosis and Viral Hepatitismentioning

confidence: 99%

“…The HCV core protein may be either pro- or antiapoptotic. This inconsistency derives from several influencing factors: genetic heterogeneity caused quasi-species HCV core proteins, activation of different signaling pathways, and diverse experimental settings 60. Similar as the dual regulatory role of HBx in hepatocyte apoptosis, activations of survival and proliferation signaling pathways are responsible for its antiapoptotic property, while a change in the mitochondrial membrane potential is usually seen when HCV core appears to be apoptotic.…”

Section: Hepatocyte Apoptosis and Viral Hepatitismentioning

confidence: 99%

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Mechanism of Hepatocyte Apoptosis

et al. 2016

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Hepatocyte apoptosis plays important roles in both the removal of external microorganisms and the occurrence and development of liver diseases. Different conditions, such as virus infection, fatty liver disease, hepatic ischemia reperfusion, and drug-induced liver injury, are accompanied by hepatocyte apoptosis. This review summarizes recent research on the mechanism of hepatocyte apoptosis involving the classical extrinsic and intrinsic apoptotic pathways, endoplasmic reticulum stress, and oxidative stress-induced apoptosis. We emphasized the major causes of apoptosis according to the characteristics of different liver diseases. Several concerns regarding future research and clinical application are also raised.

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Section: Hepatocyte Apoptosis and Viral Hepatitismentioning

confidence: 99%

Section: Hepatocyte Apoptosis and Viral Hepatitismentioning

confidence: 99%

Mechanism of Hepatocyte Apoptosis

et al. 2016

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“…A study in transgenic mice demonstrated that constitutive expression of these HCV structural and nonstructural proteins leads to the development of HCC [4]. Among these HCV proteins, the Core protein has been strongly implicated in HCC pathogenesis because of the multiple roles it plays in host cells, including engaging in cellular transformation, oxidative stress, steatosis, and anti-apoptosis [5]. Direct induction of HCC by the Core protein has been demonstrated in transgenic mice [6].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of miRNA-30c and miR-203a is associated with hepatitis C virus core protein-induced epithelial–mesenchymal transition in normal hepatocytes and hepatocellular carcinoma cells

Liu

et al. 2015

Biochemical and Biophysical Research Communications

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“…Other species of mice are totally refractory to HCC, suggesting that both the levels of expression of the viral protein and the host are important for developing cirrhosis and HCC [51]. The effect of Core appears to depend on the levels of its expression as it has been shown to activate p53 and repress p21 WAF1/Cip1/Sid1 [44,45,52]. Thus, Core appears to play a dual role in pro-and antiapoptotic effects depending on the cell system.…”

Section: Interaction Of Hcv Core Protein With P53mentioning

confidence: 99%

Interaction of Hepatitis C Viral Proteins with Cellular Oncoproteins in the Induction of Liver Cancer

Guntaka

Padala

2014

ISRN Virology

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Hepatitis C virus infection is a major health problem all over the world. A large proportion of patients infected by HCV develop liver cirrhosis or cancer. However, the mechanism(s) remain to be elucidated. Since HCV does not carry any known oncogene, it is thought that interaction between virally encoded proteins and host proteins is responsible for carcinogenesis. Many crucial interactions between HCV-encoded proteins and host proteins have been reported. In this review we focus on the interaction of viral proteins with important regulators of cell cycle-oncoproteins YB-1, p53, and cyclin D1-which play a major role in cell proliferation, apoptosis, DNA repair, and genomic stability. Genetic variants of HCV accumulate in patients and alter these interactions of host cell proteins. It is a battle between the virus and host and the final outcome depends on the winner; if the host succeeds in clearing the virus the patient may not develop serious liver diseases. On the other hand, if the virus dominates by evolving quasispecies which code for altered proteins that interact differently with host proteins, or induce mutations in host protooncogenes, then the patient may develop liver cirrhosis and/or liver cancer.

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Dual behavior of HCV Core gene in regulation of apoptosis is important in progression of HCC

Cited by 35 publications

References 35 publications

Mechanism of Hepatocyte Apoptosis

Mechanism of Hepatocyte Apoptosis

Downregulation of miRNA-30c and miR-203a is associated with hepatitis C virus core protein-induced epithelial–mesenchymal transition in normal hepatocytes and hepatocellular carcinoma cells

Interaction of Hepatitis C Viral Proteins with Cellular Oncoproteins in the Induction of Liver Cancer

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