Occult hepatitis B virus pre-S mutations lead to cell cycle dysregulation and aberrant proliferation through activation of the Akt/mTOR/Cyclin D1 signaling pathway. (IMAGE)
Caption
Employing an experimental approach involving cell transfection, Western blotting analysis, real-time quantitative PCR, flow cytometry, cell proliferation analysis, and inhibitor treatment (left panel), this study demonstrated that occult HBV infection (OBI)-associated pre-S mutations (E39K, D44N, N98T, H128R, and I161T) activate Akt/mTOR signaling pathway, up-regulate Cyclin D1 expression, promote retinoblastoma protein (Rb) phosphorylation, drive G1/S phase transition in the cell cycle, and ultimately enhance cell proliferation. Large hepatitis B surface protein (LHBs) likely plays a critical role in mediating the process (right panel). mTOR, mammalian target of rapamycin; S6K, S6 kinase; CDK, cyclin-dependent kinase.
Credit
Huizhen Sun, Ling Mei, Shi Song, Qian Su, Ying Yan, Huimin Ji, Jie Ma, Le Chang, Lunan Wang
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