fig3

Figure 3. Tumor-promoting properties of GSK3β and underlying mechanisms reported in pancreatic cancer^[156-182]. Dotted arrow: preliminary findings (by Domoto et al.). The mechanisms responsible for the respective interconnections indicated by red bidirectional arrows are shown in Table 1 and Figure 1. GSK3β: Glycogen synthase kinase 3β; NF-κB: nuclear factor κB; Bcl-2: B-cell/chronic lymphocytic leukemia lymphoma 2; hTERT: human telomerase reverse transcriptase; XIAP: X-linked inhibitor of apoptosis protein; TRAIL: tumor necrosis factor-related apoptosis-inducing ligand; JNK: c-Jun N-terminal kinase; TFEB: transcription factor EB; STAT3: signal transducer and activator of transcription 3; TP53INP1: tumor protein 53-inducible nuclear protein 1; E2F1: E2 transcription factor 1; TopBP1: topoisomerase II binding protein 1; ATR: ataxia telangiectasia and Rad3-related; Chk1: checkpoint kinase 1; FAK: focal adhesion kinase; CXCR4: C-X-C chemokine receptor type 4; MMP: matrix metalloproteinase; CXCL: C-X-C chemokine ligand; SOX2: sex-determining region Y-box transcription factor 2.