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. 2022 Jan 27;14(1):140–157. doi: 10.4254/wjh.v14.i1.140

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©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

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Tumor microenvironment in hepatocellular carcinoma. Tumor microenvironment comprising of liver sinusoidal endothelial cells, liver resident macrophages or Kupffer cells, hepatic stellate cells, hepatic dendritic cells, tumor-associated macrophages, cytokines, fibroblasts, infiltrating immune cells, pro-tumor M2 macrophages, and growth factors mediate immune suppression, immune tolerance, and immune evasion causing increased tumorigenicity with enhanced evasion, angiogenesis, metastasis, tumor growth. IL: Interleukin; TNF-α: Tumor necrosis factor-alpha; TGF-β: Transforming growth factor-beta; IFN-γ: Interferon-gamma; MMPs: Matrix metalloproteinases; PD-1: Programmed cell death protein 1; PD-L1: Programmed death-ligand 1; PGE2: Prostaglandin E2; EGF: Epidermal growth factor; VEGF: Vascular endothelial growth factor; TIM3: T-cell immunoglobulin and mucin-domain-containing molecule-3; LAG3: Lymphocyte-activation gene 3; EMT: Epithelial mesenchymal transition.