fig2

Figure 2. The molecular pathogenesis of ICC induced by inflammation. IL-6: Interleukin-6; TNF-α: tumor necrosis factor alpha; Wnt: wingless/integrated; EGFR: epidermal growth factor receptor; ErbB2: Erb-B2 receptor tyrosine kinase 2; IL-6R: interleukin-6 receptor; TNFR: tumor necrosis factor receptor; LPR: low-density lipoprotein receptor-related protein; FZD: frizzled; iNOS: inducible nitric oxide synthase; COX2: cyclooxygenase-2; miR: microRNA; IncRNA: long non-coding RNA; NO: nitric oxide; Notch: notch signaling pathway; p38: p38 mitogen-activated protein kinase; MAPK: mitogen-activated protein kinase; MAP3K8: mitogen-activated protein kinase kinase kinase 8; DNMT1: DNA methyltransferase 1; JAK-STAT3: janus kinase-signal transducer and activator of transcription 3; p44/42 MAPK: p44/p42 mitogen-activated protein kinase (also known as ERK1/ERK2); P21: cyclin-dependent kinase inhibitor 1; SOCS3: suppressor of cytokine signaling 3; Mid-1: midline 1; P16: cyclin-dependent kinase inhibitor 2A; RASSF1A: RAS-association domain family 1, isoform A; NF2: neurofibromatosis type 2; AJID: atypical junctional intercellular domain; TCF: T-cell factor; CEF: cell-free extract.