期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 20, 期 3, 页码 -出版社
MDPI
DOI: 10.3390/ijms20030581
关键词
hepatocellular carcinoma; cirrhosis; regeneration; inflammation; cytokines; genetic instability; reactive oxygen species
资金
- National Research Foundation of Korea (NRF) [2016R1A2B4013891]
- Korea government (MSIP)
- National Research Foundation of Korea [2016R1A2B4013891] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Liver cancer is the fourth leading cause of cancer-related death globally, accounting for approximately 800,000 deaths annually. Hepatocellular carcinoma (HCC) is the most common type of liver cancer, making up about 80% of cases. Liver fibrosis and its end-stage disease, cirrhosis, are major risk factors for HCC. A fibrotic liver typically shows persistent hepatocyte death and compensatory regeneration, chronic inflammation, and an increase in reactive oxygen species, which collaboratively create a tumor-promoting microenvironment via inducing genetic alterations and chromosomal instability, and activating various oncogenic molecular signaling pathways. In this article, we review recent advances in fields of liver fibrosis and carcinogenesis, and consider several molecular signaling pathways that promote hepato-carcinogenesis under the microenvironment of liver fibrosis. In particular, we pay attention to emerging roles of the Hippo-YAP/TAZ signaling pathway in stromal activation, hepatic fibrosis, and liver cancer.
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