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Review
. 2018 Aug 29:2018:8543763.
doi: 10.1155/2018/8543763. eCollection 2018.

Molecular Pathogenesis of Nonalcoholic Steatohepatitis- (NASH-) Related Hepatocellular Carcinoma

Ozlem Kutlu  1   2 , Humeyra Nur Kaleli  3 , Ebru Ozer  3
Affiliations
Review

Molecular Pathogenesis of Nonalcoholic Steatohepatitis- (NASH-) Related Hepatocellular Carcinoma

Ozlem Kutlu et al. Can J Gastroenterol Hepatol. .

Abstract

The proportion of obese or diabetic population has been anticipated to increase in the upcoming decades, which rises the prevalence of nonalcoholic fatty liver disease (NAFLD) and its progression to nonalcoholic steatohepatitis (NASH). Recent evidence indicates that NASH is the main cause of chronic liver diseases and it is an important risk factor for development of hepatocellular carcinoma (HCC). Although the literature addressing NASH-HCC is growing rapidly, limited data is available about the etiology of NASH-related HCC. Experimental studies on the molecular mechanism of HCC development in NASH reveal that the carcinogenesis is relevant to complex changes in signaling pathways that mediate cell proliferation and energy metabolism. Genetic or epigenetic modifications and alterations in metabolic, immunologic, and endocrine pathways have been shown to be closely related to inflammation, liver injury, and fibrosis in NASH along with its subsequent progression to HCC. In this review, we provide an overview on the current knowledge of NASH-related HCC development and emphasize molecular signaling pathways regarding their mechanism of action in NASH-derived HCC.

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Figures

Figure 1
Figure 1
Development of NASH and HCC from healthy liver.
Figure 2
Figure 2
The proposed mechanisms in NASH-related HCC progression.
Figure 3
Figure 3
Molecular signaling pathways involved in NASH-related HCC.
Figure 4
Figure 4
Interaction of oncogenic pathways in NASH-HCC progression.
See this image and copyright information in PMC

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