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Fig. 1. Proposed schematic illustrates driver function of SF3B4 in early hepatocarcinogenesis. At the early-stage of HCC, SF3B4 overexpression triggers aberrant splicing of KLF4 to produce non-functional transcripts, which, in turn, suppresses the wild-type tumor suppressor gene, KLF4. Resultant suppression of KLF4WT contributes to activate malignant transformation and growth of hepatocytes via disturbance of the cell cycle and epithelial–mesenchymal transition (EMT) regulation by suppressing p27kip1 and simultaneously inducing Slug expression in HCC.
BMB Reports 2018;51:57~58 https://doi.org/10.5483/BMBRep.2018.51.2.021
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