Risk of hepatocellular carcinoma after hepatitis C virus cure

Luna-Cuadros, María Alejandra; Chen, Haowei; Hanif, Hira; Ali, Mukarram Jamat; Khan, Muzammil; Lau, Daryl T.Y.

doi:10.3748/wjg.v28.i1.96

Cited by 28 publications

(17 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, in patients with cirrhosis, the risk of HCC persists even after HCV treatment. The number of patients with cirrhosis who have been cured of HCV is predicted to increase in the future [55]. Owing to dysregulated host factors during HCV infection, these patients are still at risk for liver disease development.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 regulates HCV-induced Hepatocellular carcinoma by modulating the miR-9-BGH3 axis

Tripathi

Pal

Ghosh

et al. 2022

Journal of General Virology

View full text Add to dashboard Cite

Chronic hepatitis C virus (HCV) infection is a leading cause of end-stage liver diseases, such as fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Several cellular entities, including paraspeckles and their related components, are involved in viral pathogenesis and cancer progression. NEAT1 lncRNA is a major component of paraspeckles that has been linked to several malignancies. In this study, analysis of the Cancer Genome Atlas (TCGA) database and validation in HCV-induced HCC tissue and serum samples showed significantly high expression of NEAT1 in patients with liver cancer. Moreover, we found that NEAT1 levels increased upon HCV infection. To further understand the mechanism of NEAT1-induced HCC progression, we selected one of its targets, miR-9–5 p, which regulates BGH3 mRNA levels. Interestingly, miR-9–5 p levels were downregulated upon HCV infection, whereas BGH3 levels were upregulated. Additionally, partial NEAT1 knockdown increased miR-9–5 p levels and decreased BGH3 levels, corroborating our initial results. BGH3 levels were also upregulated in HCV-induced HCC and TCGA tissue samples, which could be directly correlated with NEAT1 levels. As a known oncogene, BGH3 is directly linked to HCC progression mediated by NEAT1. We also found that NEAT1 levels remained upregulated in serum samples from patients treated with direct-acting antivirals (DAA), indicating that NEAT1 might be a molecular trigger that promotes HCC development. Collectively, these findings provide molecular insights into HCV-induced HCC progression via the NEAT1-miR-9-BGH3 axis.

show abstract

Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 regulates HCV-induced Hepatocellular carcinoma by modulating the miR-9-BGH3 axis

Tripathi

Pal

Ghosh

et al. 2022

Journal of General Virology

View full text Add to dashboard Cite

show abstract

“…Chronic HCV infection has been found as major cause of hepatocellular carcinoma. The occurrence and reoccurrence of HCC in HCV patients receiving DAAs therapy has sparked a large debate ( Tayyab et al, 2020 , Ogawa et al, 2020 , Luna-Cuadros et al, 2022 ). The clinical studies have shown that the DAAs therapy is an effective tool in reducing the risk of HCC development in cirrhotic HCV patients, however, it cannot eradicate the risk of HCC recurrence permanently ( Singer et al, 2018 , Singh et al, 2018 , Ioannou et al, 2018 , Nakano et al, 2019 , Pons et al, 2020 , Dang et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

“…The DDAs alone or in combination of other drugs have increased the SVR up to 90 percent and decreased the treatment duration up to 12 weeks ( Asselah et al, 2016 ). Debate has been emerging about the occurrence and recurrence of hepatocellular carcinoma in HCV patients receiving DAAs therapy ( Tayyab et al, 2020 , Ogawa et al, 2020 , Luna-Cuadros et al, 2022 ). Over the time, a series of clinical studies reported the efficacy of DAAs therapy in reducing the risk of HCC development in cirrhotic HCV patients.…”

Section: Introductionmentioning

confidence: 99%

Targeting the effect of sofosbuvir on selective oncogenes expression level of hepatocellular carcinoma Ras/Raf/MEK/ERK pathway in Huh7 cell line

Atif

Mustaan

Falak³

et al. 2022

Saudi Journal of Biological Sciences

View full text Add to dashboard Cite

“…Some of these mechanisms may persist even after HCV eradication, and thus the risk of HCC development is not abolished. This is still a hotly discussed subject [ 154 , 161 ].…”

Section: Hcc Related To Specific Diseasesmentioning

confidence: 99%

Pathogenesis of Hepatocellular Carcinoma: The Interplay of Apoptosis and Autophagy

2023

View full text Add to dashboard Cite

The pathogenesis of hepatocellular carcinoma (HCC) is a multifactorial process that has not yet been fully investigated. Autophagy and apoptosis are two important cellular pathways that are critical for cell survival or death. The balance between apoptosis and autophagy regulates liver cell turnover and maintains intracellular homeostasis. However, the balance is often dysregulated in many cancers, including HCC. Autophagy and apoptosis pathways may be either independent or parallel or one may influence the other. Autophagy may either inhibit or promote apoptosis, thus regulating the fate of the liver cancer cells. In this review, a concise overview of the pathogenesis of HCC is presented, with emphasis on new developments, including the role of endoplasmic reticulum stress, the implication of microRNAs and the role of gut microbiota. The characteristics of HCC associated with a specific liver disease are also described and a brief description of autophagy and apoptosis is provided. The role of autophagy and apoptosis in the initiation, progress and metastatic potential is reviewed and the experimental evidence indicating an interplay between the two is extensively analyzed. The role of ferroptosis, a recently described specific pathway of regulated cell death, is presented. Finally, the potential therapeutic implications of autophagy and apoptosis in drug resistance are examined.

show abstract

Risk of hepatocellular carcinoma after hepatitis C virus cure

Cited by 28 publications

References 73 publications

LncRNA NEAT1 regulates HCV-induced Hepatocellular carcinoma by modulating the miR-9-BGH3 axis

LncRNA NEAT1 regulates HCV-induced Hepatocellular carcinoma by modulating the miR-9-BGH3 axis

Targeting the effect of sofosbuvir on selective oncogenes expression level of hepatocellular carcinoma Ras/Raf/MEK/ERK pathway in Huh7 cell line

Pathogenesis of Hepatocellular Carcinoma: The Interplay of Apoptosis and Autophagy

Contact Info

Product

Resources

About