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Autophagy in the “inflammation-carcinogenesis” pathway of liver and HCC immunotherapy

  • Sizhe Yu
  • , Yu Wang
  • , Li Jing
  • , F. X. Claret
  • , Qing Li
  • , Tao Tian
  • , Xuan Liang
  • , Zhiping Ruan
  • , Lili Jiang
  • , Yu Yao
  • , Kejun Nan
  • , Yi Lv
  • , Hui Guo
  • The First Affiliated Hospital of Xi’an Jiaotong University
  • University of Texas MD Anderson Cancer Center

Research output: Contribution to journalReview articlepeer-review

63 Scopus citations

Abstract

Autophagy plays a dual role in many types of cancer, such as hepatocellular carcinoma (HCC). Autophagy seems to be inhibited and functions as a tumor-suppression mechanism in the “inflammation-carcinogenesis” pathway of the liver, including hepatitis B virus and hepatitis C virus, alcoholic steatohepatitis and non-alcoholic steatohepatitis related HCC. However, in established tumors, autophagy plays a tumor-promoting role. Because of the varied function of autophagy in HCC, we hypothesized p62 as a marker to evaluate the autophagic level. Moreover, autophagy is critical in antigen presentation and homeostasis of immune cells and tumor microenvironment. Understanding the intricate relationships of autophagy, inflammation, and immunity provides us with new insights into HCC immunotherapy.

Original languageEnglish
Pages (from-to)82-89
Number of pages8
JournalCancer Letters
Volume411
DOIs
StatePublished - 28 Dec 2017
Externally publishedYes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Autophagy
  • Hepatocellular carcinoma
  • Immunotherapy
  • Inflammation

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