TABLE 8.
Cells | The research direction | Result | Reference |
---|---|---|---|
M2-polarized macrophages | The immune mechanism | MicroRNA (miR-17-92) clusters from the extracellular vesicles (EVs) of M2-polarized tumor-associated macrophages (M2-TAMs) stimulate the imbalance of the TGF-β1/BMP-7 pathway, TGF-β1/BMP-7 pathway imbalance significantly promotes HCC cell invasion and stem cells by increasing the expression of differentiation inhibitor 1(ID1). | Ning et al. (2021) |
M2-polarized macrophages | The immune mechanism | Elevated levels of Mir-15B are transferred from arsenite-treated THP-1 (AS-THP-1) cells to HCC cells via Mir-15b in EVs, inhibit Hippo pathway activation by targeting LATS1, and participate in the migration and invasion of proliferation-promoting HCC cells. | Li et al. (2021) |
M2-polarized macrophages | The immune mechanism | β2-AR promotes the occurrence and development of HCC by silencing GRK2 in M2 polarized macrophages. | Wu et al. (2019b) |
M2-polarized macrophages | immunotherapy | Tumor cell-derived Wnt ligands stimulate M2-like polarization of TAM through classical Wnt/β-catenin signaling, which leads to tumor growth, migration, metastasis, and immunosuppression in HCC. | Yang et al. (2018a) |
M2-polarized macrophages | immunotherapy | M2-polarized macrophages promote the migration and EMT of HCC cells through the TLR4/STAT3 signaling pathway, suggesting that TLR4 may be a new therapeutic target. | Yao et al. (2018) |