2017
DOI: 10.1111/cas.13117
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NS5ABP37 inhibits liver cancer by impeding lipogenesis and cholesterogenesis

Abstract: The molecular mechanism underlying non‐alcoholic fatty liver disease progression to hepatocellular carcinoma (HCC) remains unknown. In this study, immunohistochemistry staining results showed that NS5ABP37 protein, which is in a state of lower expression in tumor tissues, decreased with increasing degree of HCC malignancy. Two cell models, HepG2 and L02, were used to analyze the mechanism between NS5ABP37 and HCC. In agreement, NS5ABP37 protein overexpression significantly suppressed cell proliferation, caused… Show more

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Cited by 6 publications
(4 citation statements)
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“…Overexpression of NS5ABP37protein, a HCC oncogenomic screen and hepatitis C virus nonstructural protein 5A‐associated binding protein, decreased intracellular triglyceride and total cholesterol contents, down-regulated SREBP1c and SREBP2 expression and inhibited cancer cell proliferation in human hepatoma cells. 99 Moreover, SREBP pathway blocking by L-Scap-/- and L-gp78-/- mice led to reduced SREBP1c, SREBP1a and SREBP2 expression and to decrease in related enzymes, such as fatty acid synthase, ACC, LDLR and HMGCs, improving HCC tumor progression. 100 In human NAFLD-associated HCC, SREBP-1 up-regulated HDAC8 and suppression of the histone deacetylase HDAC8, and decreased insulin resistance and NAFLD-associated HCC.…”
Section: Srebps In Liver Diseasementioning
confidence: 96%
“…Overexpression of NS5ABP37protein, a HCC oncogenomic screen and hepatitis C virus nonstructural protein 5A‐associated binding protein, decreased intracellular triglyceride and total cholesterol contents, down-regulated SREBP1c and SREBP2 expression and inhibited cancer cell proliferation in human hepatoma cells. 99 Moreover, SREBP pathway blocking by L-Scap-/- and L-gp78-/- mice led to reduced SREBP1c, SREBP1a and SREBP2 expression and to decrease in related enzymes, such as fatty acid synthase, ACC, LDLR and HMGCs, improving HCC tumor progression. 100 In human NAFLD-associated HCC, SREBP-1 up-regulated HDAC8 and suppression of the histone deacetylase HDAC8, and decreased insulin resistance and NAFLD-associated HCC.…”
Section: Srebps In Liver Diseasementioning
confidence: 96%
“…TG are composed of 3 fatty acids (FA) and glycerol, and their accumulation is the hallmark of NASH, resulting in hepatic dysfunction, such as insulin resistance . Previous studies have demonstrated that hepatic TG themselves are not toxic and may protect the liver from FA‐induced lipotoxicity, but lipogenesis has an important role in cellular survival of HCC . However, the toxic effects of FA on hepatic cancer cells have not yet been examined in detail.…”
Section: Introductionmentioning
confidence: 99%
“…Cellular cholesterol synthesis is enhanced in liver cancer cells, and sterol regulatory element-binding transcription factor 2 and low-density lipoprotein receptor expression are induced (29). Higher endogenous cholesterol biosynthesis and uptake of low-density lipoprotein particles are essential for cell proliferation and survival (30). Blocking acyl-CoA cholesterol acyltransferase-1 suppresses proliferation and induces apoptosis of cancer cells, and this is attributed to the cytotoxic effects of free cholesterol (31).…”
Section: Discussionmentioning
confidence: 99%