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自噬在肝和 HCC 免疫治疗的“炎症-致癌”通路中的作用。

Autophagy in the "inflammation-carcinogenesis" pathway of liver and HCC immunotherapy.

机构信息

Department of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, PR China.

Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

出版信息

Cancer Lett. 2017 Dec 28;411:82-89. doi: 10.1016/j.canlet.2017.09.049. Epub 2017 Oct 5.

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.

摘要

自噬在多种类型的癌症中发挥双重作用,例如肝细胞癌(HCC)。自噬似乎受到抑制,并在肝脏的“炎症-致癌”途径中发挥肿瘤抑制机制的作用,包括乙型肝炎病毒和丙型肝炎病毒、酒精性脂肪性肝炎和非酒精性脂肪性肝炎相关 HCC。然而,在已建立的肿瘤中,自噬起促进肿瘤的作用。由于自噬在 HCC 中的功能多样,我们假设 p62 作为评估自噬水平的标志物。此外,自噬在免疫细胞和肿瘤微环境的抗原呈递和稳态中至关重要。了解自噬、炎症和免疫之间的复杂关系为 HCC 免疫治疗提供了新的见解。

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