Journal
SEMINARS IN LIVER DISEASE
Volume 39, Issue 1, Pages 26-42Publisher
THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0038-1676806
Keywords
NF-kappa B; apoptosis; hepatic stellate cells; ER stress; immune checkpoint inhibitor
Categories
Funding
- National Institutes of Health (NIH) [R01DK085252, R01AA027036, R21AA025841, T32HL134637]
- American Liver Foundation (ALF)
- Cedars-Sinai Medical Center
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Hepatocellular carcinoma (HCC) is associated with chronic inflammation and fibrosis arising from different etiologies, including hepatitis B and C and alcoholic and nonalcoholic fatty liver diseases. The inflammatory cytokines tumor necrosis factor-alpha and interleukin-6 and their downstream targets nuclear factor kappa B (NF-kappa B), c-Jun N-terminal kinase (JNK), and signal transducer and activator of transcription 3 drive inflammation-associated HCC. Further, while adaptive immunity promotes immune surveillance to eradicate early HCC, adaptive immune cells, such as CD8(+) T cells, Th17 cells, and B cells, can also stimulate HCC development. Thus, the role of the hepatic immune system in HCC development is a highly complex topic. This review highlights the role of cytokine signals, NF-kappa B, JNK, innate and adaptive immunity, and hepatic stellate cells in HCC and discusses whether these pathways could be therapeutic targets. The authors will also discuss cholangiocarcinoma and liver metastasis because biliary inflammation and tumor-associated stroma are essential for cholangiocarcinoma development and because primary tumor-derived inflammatory mediators promote the formation of a premetastasis niche in the liver.
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