scholarly journals Tobacco Smoking and Liver Cancer Risk: Potential Avenues for Carcinogenesis

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Divya Jain ◽  
Priya Chaudhary ◽  
Nidhi Varshney ◽  
Khandaker Sabit Bin Razzak ◽  
Devret Verma ◽  
...  
Keyword(s):  
Hepatitis C ◽  
Liver Cancer ◽  
Common Factor ◽  
Premature Death ◽  
Heavy Smoking ◽  
Tnf Α ◽  
Proliferation Of Lymphocytes ◽  
Ifn Therapy ◽  
Risk Potential ◽  
Necrosis Factor

Smoking a cigarette generates over 4000 chemicals that have a deleterious impact on each part of the human body. It produces three main severe effects on the liver organ: oncogenic, immunological, and indirect or direct toxic effects. It results in the production of cytotoxic substances, which raises fibrosis and necro-inflammation. Additionally, it also directs the production of pro-inflammatory cytokines tumour necrosis factor alfa (TNF-α) and interleukins (IL-1β, IL-6) that will be responsible for the chronic liver injury. Furthermore, it gives rise to secondary polycythemia and successively raises the turnover and mass of red cells, which might be a common factor responsible for the development of oxidative stress in the liver due to iron overload. It also produces chemicals that are having oncogenic properties and raises the risk of liver cancer especially in sufferers of chronic hepatitis C. Smoking modulates both humoral and cell-mediated responses by restricting the proliferation of lymphocytes and inducing their apoptosis and ultimately decreasing the surveillance of cancer cells. Moreover, it has been determined that heavy smoking impacts the response of hepatitis C patients to interferon (IFN) therapy through different mechanisms, which can be improved by phlebotomy. Efforts are being made in different nations in decreasing the prevalence of smoking to improve premature death and ill effects of their nation’s individuals.

scholarly journals Hepatitis C Virus Nonstructural 5B Protein Regulates Tumor Necrosis Factor Alpha Signaling through Effects on Cellular IκB Kinase

2006 ◽  
Vol 26 (8) ◽  
pp. 3048-3059 ◽  
Author(s):  
Soo-Ho Choi ◽  
Kyu-Jin Park ◽  
Byung-Yoon Ahn ◽  
Guhung Jung ◽  
Michael M. C. Lai ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Hepatic Cells ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ns5b Protein ◽  
Necrosis Factor

ABSTRACT Hepatitis C virus (HCV) NS5B protein is a membrane-associated phosphoprotein that possesses an RNA-dependent RNA polymerase activity. We recently reported that NS5A protein interacts with TRAF2 and modulates tumor necrosis factor alpha (TNF-α)-induced NF-κB and Jun N-terminal protein kinase (JNK). Since NS5A and NS5B are the essential components of the HCV replication complex, we examined whether NS5B could modulate TNF-α-induced NF-κB and JNK activation. In this study, we have demonstrated that TNF-α-induced NF-κB activation is inhibited by NS5B protein in HEK293 and hepatic cells. Furthermore, NS5B protein inhibited both TRAF2- and IKK-induced NF-κB activation. Using coimmunoprecipitation assays, we show that NS5B interacts with IKKα. Most importantly, NS5B protein in HCV subgenomic replicon cells interacted with endogenous IKKα, and then TNF-α-mediated IKKα kinase activation was significantly decreased by NS5B. Using in vitro kinase assay, we have further found that NS5B protein synergistically activated TNF-α-mediated JNK activity in HEK293 and hepatic cells. These data suggest that NS5B protein modulates TNF-α signaling pathways and may contribute to HCV pathogenesis.

scholarly journals Inhibition of Tumor Necrosis Factor (TNF-α)-mediated Apoptosis by Hepatitis C Virus Core Protein

1998 ◽  
Vol 273 (4) ◽  
pp. 2256-2259 ◽  
Author(s):  
Ratna B. Ray ◽  
Keith Meyer ◽  
Robert Steele ◽  
Anju Shrivastava ◽  
Bharat B. Aggarwal ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Core Protein ◽  
Virus Core ◽  
Tnf Α ◽  
Necrosis Factor

Radix Bupleuri Containing Compound (KY88 Liver-Livo) Induces Apoptosis and Production of Interleukin-4 and Tumor Necrosis Factor-α in Liver Cancer Cellsin Vitro

2004 ◽  
Vol 32 (02) ◽  
pp. 185-193 ◽  
Author(s):  
Louis W.C. Chow ◽  
Wings T.Y. Loo ◽  
Jonathan S.T. Sham ◽  
Mary N.B. Cheung
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Necrosis Factor ◽  
Liver Cancer ◽  
Tumor Necrosis ◽  
Interleukin 4 ◽  
Dna Ladder ◽  
Tnf Α ◽  
Radix Bupleuri ◽  
Factor Α ◽  
Necrosis Factor

Hepatocellular carcinoma is an important health problem in Asia. A blend of herbal extracts containing radix bupleuri (KY88) was tested for its effects on liver cancer cells. A hepatocellular carcinoma cell line (HB8064) was cultured with methanol extract of KY88. We were able to produce a dose-dependent inhibition of cancer cell proliferation. At IC50and IC100, KY88 induces a DNA ladder pattern, indicating the presence of apoptosis. We also checked the changes of the levels of interleukin (IL)-2, -4 and -6, interferon (INF)-γ and tumor necrosis factor (TNF)-α by ELISA kits. After 24 hours of culture, there was activation of IL-2 and -4 and TNF-α. However, significant changes were observed only for IL-4 and TNF-α. Therefore, we concluded that KY88 is able to induce apoptosis, which may be regulated through changes in IL-4 and TNF-α.

scholarly journals Increase Serum Tumor Necrosis Factor Alpha decreased Serum Cholesterol Level, but not Albumin, in Hemodialysis Patients with Non-Fibrotic Hepatitis C Infection

2021 ◽  
Vol 9 (B) ◽  
pp. 614-619
Author(s):  
Rudi Supriyadi ◽  
Nenny Agustanti ◽  
Marcella Adisuhanto
Keyword(s):  
Chronic Kidney Disease ◽  
Hepatitis C ◽  
Kidney Disease ◽  
Hepatitis C Infection ◽  
Infection Group ◽  
Necrosis Factor Alpha ◽  
Cholesterol Levels ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

BACKGROUND: Hepatitis C infection could increase the morbidity and mortality of chronic kidney disease patients on hemodialysis by enhancing the inflammatory process. Tumor Necrosis Factor-alpha (TNF-a) is the main regulator of the inflammatory cascade, which could induce malnutrition and suppress cholesterol and albumin production in the liver. AIM: Therefore, this study aimed to determine the correlation between serum TNF-a level with serum albumin and cholesterol levels in chronic kidney disease patients on hemodialysis with and without hepatitis C infection. METHODS: This research was an analytical cross-sectional study. The sample of this study consisted of patients undergoing routine hemodialysis at Dr. Hasan Sadikin Hospital, Bandung, in February 2020. The sample selection was using a random sampling method and analyzed with the Spearman rank correlation test. RESULTS: One hundred nineteen patients were divided into two groups, with hepatitis C infection (n=53) and without hepatitis C infection (n=66). The median value of serum TNF-α _was higher in the hepatitis C infection group compared to the group without hepatitis c infection (31.86 pg/ml vs 11.71 pg/ml, p <0.001). There was a correlation between serum TNF-α _and cholesterol in the hepatitis C infection (r = -0.246; p = 0.039) and without hepatitis c infection group (r = -0.256; p = 0.022). After adjusting with the duration of hemodialysis, this association was found to be significant in patients without Hepatitis C infection (p = 0.02) and borderline significant in patients with Hepatitis C infection (p = 0.09). There was no correlation between TNF-α _with albumin in both hepatitis C infection group (r = 0.082; p = 0.281) and without hepatitis C infection (r = -0.168; p = 0.094). CONCLUSION: Serum TNF-α _negatively correlates with cholesterol levels in chronic kidney disease patients on hemodialysis with and without hepatitis C infection. However, there was no correlation between TNF-α _and albumin level in both groups.

scholarly journals Hepatitis C Virus Core Protein Inhibits Fas- and Tumor Necrosis Factor Alpha-Mediated Apoptosis via NF-κB Activation

1999 ◽  
Vol 73 (6) ◽  
pp. 4713-4720 ◽  
Author(s):  
Hiroyuki Marusawa ◽  
Makoto Hijikata ◽  
Tsutomu Chiba ◽  
Kunitada Shimotohno
Keyword(s):  
Cell Death ◽  
Hepatitis C ◽  
Tumor Necrosis ◽  
Core Protein ◽  
Apoptotic Cell ◽  
Necrosis Factor Alpha ◽  
The Core ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The effects of hepatitis C virus (HCV) proteins on anti-Fas (CD95/APO-1) antibody- and tumor necrosis factor alpha (TNF-α)-mediated apoptosis in different human cell lines were investigated by magnetic concentration of cells which transiently produced the exogenous protein. HepG2 cells, which produced whole HCV proteins, became resistant to anti-Fas-induced apoptotic cell death. Furthermore, the core protein among HCV proteins had a key role in protecting the various cells from apoptosis mediated by not only anti-Fas but also TNF-α. We also found that the core functioned in the activation of nuclear factor κB (NF-κB) in all cells examined. Deletion analysis of the core revealed that the region required for NF-κB activation was closely correlated with that for its antiapoptotic function. In addition, we revealed in some cases that the antiapoptotic effect of the core was restrained by coproduction of the inhibitor of NF-κB, IκB-α protein. These results demonstrated that the core inhibits Fas- and TNF-α-mediated apoptotic cell death via a mechanism dependent on the activation of NF-κB in particular cell lines.

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