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c-met/β-catenin-driven hepatocarcinogenesis wnt/β-catenin signaling pathway itgb1-fak-akt signaling pathway month download article/chapter integrin α2β1-mediated fak egfr-erk1/2 signaling pathway virus-mediated chd1l depletion virus-related hepatocellular carcinoma fak-akt signaling activation anti-tumor dendritic cells explorative cgh meta-analysis inducing epithelial-mesenchymal transition rab-5-dependent endocytic transport activating fak-akt signaling phospho-fak p-akt kaplan–meier survival analysis liver hepatocellular carcinoma sm protein vps-45 full article pdf endocytic recycling pathway amplified dna sequences english language editing recycling β1 integrin β1 integrin recycling privacy choices/manage cookies advanced hepatocellular carcinoma including vps45 knockout sustain tumor growth phospho-akt qpcr hepatocellular carcinoma detected related subjects nat rev cancer promotes oncogenic phenotypes nucleocytoplasmic shuttling protein electronic supplementary material promotes tumor progression intertwining molecular networks accepted manuscript version exp cell res nat cell biol survival p-fak drive malignant phenotypes hepatocellular carcinoma progression yap-dependent manner holds exclusive rights cancer genome atlas article journal chromosome 1q21 amplification western blot analysis flow cytometric analysis

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         headline:VPS45 promotes the progression of hepatocellular carcinoma by recycling β1 integrin to the cell membrane via the endocytic pathway
         description:Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with poor prognosis, which is often driven by chromosomal amplifications at 1q. Vacuolar sorting protein 45 (VPS45), a gene located on chromosome 1q, is involved in the endocytic recycling pathway; however, its role in HCC remains unclear. In this study, we aimed to investigate the functional significance of VPS45 in the progression of HCC. VPS45 expression was analyzed using public databases, clinical HCC samples, and cell lines. Functional assays, including VPS45 knockout and rescue experiments, were conducted to assess the effect on tumor progression in vitro and in vivo. The molecular mechanisms underlying VPS45 function, particularly its role in β1 integrin recycling and FAK-AKT signaling activation, were also explored. VPS45 expression was significantly elevated in HCC owing to DNA copy number amplification and correlated with poor prognosis. Moreover, VPS45 knockout suppressed cell proliferation, migration, and invasion, while promoting apoptosis. VPS45 interacted with syntaxin16 and rabenosyn-5 to facilitate the recycling of β1 integrin to the cell membrane, thereby activating FAK-AKT signaling, which promotes oncogenic phenotypes. In xenograft models, VPS45 knockout significantly suppressed tumor growth, further supporting its role in HCC progression. VPS45 is a key oncogene in HCC that promotes tumor progression by enhancing β1 integrin recycling and activating FAK-AKT signaling. Given its strong association with poor prognosis and tumor malignancy, VPS45 may serve as a promising prognostic biomarker and a potential therapeutic target for HCC.
         datePublished:2025-06-20T00:00:00Z
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            Vacuolar sorting protein 45 (VPS45)
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      description:Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with poor prognosis, which is often driven by chromosomal amplifications at 1q. Vacuolar sorting protein 45 (VPS45), a gene located on chromosome 1q, is involved in the endocytic recycling pathway; however, its role in HCC remains unclear. In this study, we aimed to investigate the functional significance of VPS45 in the progression of HCC. VPS45 expression was analyzed using public databases, clinical HCC samples, and cell lines. Functional assays, including VPS45 knockout and rescue experiments, were conducted to assess the effect on tumor progression in vitro and in vivo. The molecular mechanisms underlying VPS45 function, particularly its role in β1 integrin recycling and FAK-AKT signaling activation, were also explored. VPS45 expression was significantly elevated in HCC owing to DNA copy number amplification and correlated with poor prognosis. Moreover, VPS45 knockout suppressed cell proliferation, migration, and invasion, while promoting apoptosis. VPS45 interacted with syntaxin16 and rabenosyn-5 to facilitate the recycling of β1 integrin to the cell membrane, thereby activating FAK-AKT signaling, which promotes oncogenic phenotypes. In xenograft models, VPS45 knockout significantly suppressed tumor growth, further supporting its role in HCC progression. VPS45 is a key oncogene in HCC that promotes tumor progression by enhancing β1 integrin recycling and activating FAK-AKT signaling. Given its strong association with poor prognosis and tumor malignancy, VPS45 may serve as a promising prognostic biomarker and a potential therapeutic target for HCC.
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      name:Takaaki Masuda
      affiliation:
            name:Kochi University
            address:
               name:Department of Breast and Endocrine Surgery, Kochi University, Kochi, Japan
               type:PostalAddress
            type:Organization
      name:Hiromitsu Hayashi
      affiliation:
            name:Kumamoto University
            address:
               name:Department of Gastroenterological Surgery, Graduate School of Medicine, Kumamoto University, Kumamoto, Japan
               type:PostalAddress
            type:Organization
      name:Masaaki Iwatsuki
      affiliation:
            name:Kumamoto University
            address:
               name:Department of Gastroenterological Surgery, Graduate School of Medicine, Kumamoto University, Kumamoto, Japan
               type:PostalAddress
            type:Organization
      name:Koshi Mimori
      affiliation:
            name:Kyushu University Beppu Hospital
            address:
               name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Gastroenterological Surgery, Graduate School of Medicine, Kumamoto University, Kumamoto, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
      name:Department of Breast and Endocrine Surgery, Kochi University, Kochi, Japan
      name:Department of Gastroenterological Surgery, Graduate School of Medicine, Kumamoto University, Kumamoto, Japan
      name:Department of Gastroenterological Surgery, Graduate School of Medicine, Kumamoto University, Kumamoto, Japan
      name:Department of Surgery, Kyushu University Beppu Hospital, Beppu Oita, Japan
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

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