Crosstalk and the progression of hepatocellular carcinoma.
- Author:
Lei-Rong GU
1
;
Hui ZHANG
1
;
Juan CHEN
1
;
Sheng-Tao CHENG
1
Author Information
- Publication Type:English Abstract
- MeSH: Humans; Carcinoma, Hepatocellular/metabolism*; Liver Neoplasms/metabolism*; Hepatic Stellate Cells/physiology*; Disease Progression; Signal Transduction/physiology*; Transforming Growth Factor beta/metabolism*; Cell Proliferation; Hedgehog Proteins/metabolism*; Tumor-Associated Macrophages; Platelet-Derived Growth Factor/metabolism*; Cell Communication/physiology*
- From: Acta Physiologica Sinica 2025;77(2):267-276
- CountryChina
- Language:Chinese
- Abstract: Malignant proliferating liver cancer cells possess the ability to detect and respond to various body signals, thereby facilitating tumor growth, invasion, and metastasis. One crucial mechanism through which hepatocellular carcinoma (HCC) cells interpret these signals is crosstalk. Within liver cancer tissues, cancer cells engage in communication with hepatic stellate cells (HSCs), tumor-associated macrophages (TAMs), and immune cells. This interaction plays a pivotal role in regulating the proliferation, invasion, and metastasis of HCC cells. Crosstalk occurs in multiple ways, each characterized by distinct functions. Its molecular mechanisms primarily involve regulating immune cell functions through the expression of specific receptors, such as CD24 and CD47, modulating cell functions by secreting cytokines like transforming growth factor-β (TGF-β) and platelet-derived growth factor (PDGF), and mediating cell growth and proliferation by activating pathways such as Wnt/β-catenin and Hedgehog. A comprehensive understanding of the mechanisms and interactions within crosstalk is essential for unraveling the pathogenesis of HCC. It also opens up new avenues for the development of innovative therapeutic strategies. This article reviews the relationship between crosstalk and the progression of HCC, offering insights and inspiration for future research.
