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. 2020 Jul 16;9(7):2255. doi: 10.3390/jcm9072255

Figure 3.

Figure 3

The contributions of the tumor microenvironments and other regulators to the activation of EGFR in cholangiocarcinoma. Secretion of heparin-binding EGF-like growth factor (HB-EGF) by human liver myofibroblasts (HLMF’s) and elevated levels of bile acids from the liver can be overstimulating EGFR in paracrine fashions. EGFR can also be activated by secretion of transforming growth factor (TGF)-β1, the trefoil factor family (TFF) 2, prostaglandin (PGE) 2 in an autocrine fashion, which is produced by the CC cells. Moreover, other positive or negative regulators are involved in the regulation of EGFR activation by direct interaction. TGFα: Transforming growth factor-α, HB-EGF: EGF-like growth factor, TLCA: Taurolithocholic acid, TCA: Taurocholic acid, S1PR2: Sphingosine 1-phosphate receptor 2, M3 mAChR: Muscarinic acetylcholine receptor M3, FUT1: fucosyltransferase 1, LAMC2: Laminin subunit gamma 2, NF2: Neurofibromatosis type 2, EBP50: SLC9A3 regulator 1, EP1: Prostaglandin E receptor 1, TFF2: Trefoil factor family 2, GSK3β: Glycogen synthase kinase 3, MCL1: MCL1 apoptosis regulator, SOX4: SRY-box transcription factor 4, COX2: Cyclooxygenase 2, TGF-β1: Transforming growth factor- β1.