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In the early stage, DPI, miR146b and Fgl2 inhibit M1 polarization, and Fgl2 promote M2 polarization, which both inhibit the tumorigenesis of CAC. XOR promotes M1 polarization and enhance the tumor progression of CAC. In the later stage, vitexin promotes M1 polarization, IL-28B and Embelin inhibit M2 polarization, which both inhibit CAC progress. TRPV1, HCK and OPN promote M2 polarization and enhance the tumor progression of CAC.
