Roles of conventional and complementary therapies in recurrent hepatocellular carcinoma

Figure 1 Summary of molecular pathways involved in complementary therapies in recurrent hepatocellular carcinoma. Akt: Protein kinase B; AMPK: AMP-activated protein kinase; Bax: BCL2-Associated X Protein; Bcl-2: B-cell lymphoma 2; CD: Cluster of differentiation; EpCAM: Epithelial cell adhesion molecule; ERK: Extracellular signal-regulated kinase; FoxO: Forkhead box O; GSK: Glycogen synthase kinase; HCC: Hepatocellular carcinoma; HOTTIP: HOXA distal transcript antisense RNA; JNK: c-Jun N-terminal kinase; MAPK: Mitogen-activated protein kinase; MCL-1: Myeloid cell leukemia 1; MMP: Matrix metalloproteinase; mTOR: Mammalian target of rapamycin; MUC1: Mucin 1; NF-κB: Nuclear factor kappa B; PI3K: Phosphatidylinositol 3-kinase; PTEN: Phosphatase and tensin homolog deleted on chromosome 10; PTTG1: Pituitary tumor transforming gene 1; RAF: Rapidly accelerated fibrosarcoma; STAT3: Signal transducer and activator of transcription 3; TGF: Transforming growth factor; TUG1: Taurine upregulated 1.