Abstract
Hepatitis C virus (HCV) infections can cause permanent liver-related diseases, including hepatocellular carcinoma (HCC). Low mortality and incidence of HCC have been observed in patients with chronic hepatitis C undergoing direct-acting antiviral therapy. Tumor suppressive let-7 family members are down-regulated in HCC. The present study, therefore, aimed to investigate whether expression levels for the full spectrum of let-7 family members (let-7a, 7b, 7c, 7d, 7e, 7f, 7g, 7i, and miR-98) in the circulatory system are useful as surveillance biomarkers for liver-related diseases to monitor treatment efficacy during HCV infection. To this end, we measured the levels of mature circulating let-7 family members using quantitative reverse transcription-PCR in 236 patients with HCV infection, and 147 age- and sex-matched controls. Using hierarchical cluster analysis and principal component analysis, three clusters were obtained after measuring expression levels of let-7 family members in the patients and controls. Cluster 1 included let-7a/d/e/g, Cluster 2 comprised let-7b and let-7i, and Cluster 3 comprised let-7c/f/miR-98. Let-7b/c/g represented the three clusters and showed the best survival response to liver cancer when analyzed with respect to patient data. Therefore, considering the circulating levels of let7 b/c/g as representatives of the let-7 family may facilitate effective monitoring of liver-related disease.
Highlights
Chronic hepatitis C (CHC) virus infection can cause serious liver disorders
We examined the potential for use of nine mature let-7 family members as non-invasive biomarkers for CHC patients, using cluster analysis and principal component analysis (PCA)
[18]; they have been shown to be useful for cancer detection
Summary
Chronic hepatitis C (CHC) virus infection can cause serious liver disorders. It can increase the risk of hepatocellular carcinoma (HCC) and the progression of severe hepatic and extrahepatic diseases [1]. Resulting from treatment with pegylated interferon-α (PegIFNα) and ribavirin (RBV) is associated with a lower risk of HCC development [2]. Patients with significant hepatic fibrosis remain at high risk for HCC, even when they achieve SVR with antiviral therapy [3,4]. Since 2013, the development of direct-acting antivirals (DAAs) has increased SVR rates by 95% above those of interferon (IFN)-based treatments in patients with chronic HCV infection regardless of viral genotype [5]. There is no evidence that HCC occurrence or recurrence differs between patients receiving DAA or IFN therapy [6]
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