2024 | Deming Li, Ting Zhang, Ye Guo, Cong Bi, Ming Liu, Gang Wang
This review article explores the role of tumor-associated macrophages (TAMs) in the progression of hepatocellular carcinoma (HCC), highlighting their significant impact on tumor growth, invasion, and metabolic reprogramming. TAMs, predominantly in M2 polarization, contribute to HCC progression by secreting factors that promote glycolysis and tumor malignancy. The conversion of TAMs from M2 to M1 polarization is a potential therapeutic target, with various drugs and compounds targeting TAMs to suppress their M2 phenotype and tumorigenic activity. TAMs also facilitate cell-cell communication through exosome secretion, influencing tumor progression and therapy resistance. Non-coding RNAs play a key role in regulating TAM polarization in HCC. The tumor microenvironment (TME) is crucial for HCC progression, with TAMs interacting with HCC cells to modulate the TME and promote malignancy. Factors such as hypoxia, inflammation, and metabolic reprogramming are involved in TAM polarization and tumor progression. The review also discusses the role of macrophages in HCC immunity, therapy resistance, and the potential of targeting TAMs for improved treatment outcomes. Strategies for regulating TAMs in HCC include suppressing monocyte recruitment, modulating macrophage polarization, and using anti-tumor compounds to suppress TAMs and enhance anti-tumor immunity. The review emphasizes the importance of understanding TAMs in HCC and developing targeted therapies to improve patient outcomes.This review article explores the role of tumor-associated macrophages (TAMs) in the progression of hepatocellular carcinoma (HCC), highlighting their significant impact on tumor growth, invasion, and metabolic reprogramming. TAMs, predominantly in M2 polarization, contribute to HCC progression by secreting factors that promote glycolysis and tumor malignancy. The conversion of TAMs from M2 to M1 polarization is a potential therapeutic target, with various drugs and compounds targeting TAMs to suppress their M2 phenotype and tumorigenic activity. TAMs also facilitate cell-cell communication through exosome secretion, influencing tumor progression and therapy resistance. Non-coding RNAs play a key role in regulating TAM polarization in HCC. The tumor microenvironment (TME) is crucial for HCC progression, with TAMs interacting with HCC cells to modulate the TME and promote malignancy. Factors such as hypoxia, inflammation, and metabolic reprogramming are involved in TAM polarization and tumor progression. The review also discusses the role of macrophages in HCC immunity, therapy resistance, and the potential of targeting TAMs for improved treatment outcomes. Strategies for regulating TAMs in HCC include suppressing monocyte recruitment, modulating macrophage polarization, and using anti-tumor compounds to suppress TAMs and enhance anti-tumor immunity. The review emphasizes the importance of understanding TAMs in HCC and developing targeted therapies to improve patient outcomes.