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<p>Growing evidence highlights the critical involvement of the ubiquitin-proteasome system in cancer development. As an essential component of the 26&#xa0;S proteasome, Proteasome 26&#xa0;S Subunit ATPase 2 (PSMC2) has been implicated in various malignancies, but its role in hepatocellular carcinoma (HCC) progression remains poorly understood. We analyzed PSMC2 expression using The Cancer Genome Atlas database (TCGA) database, and validated findings in clinical HCC specimens and cell lines through immunohistochemistry (IHC) and Western blot. Functional assays (CCK-8, colony formation, Scratch test and transwell invasion assay) were performed to assess the oncogenic properties of PSMC2 in the progression of HCC. Mechanistic studies employed co-immunoprecipitation, Western blot, immunofluorescence and in vivo xenograft models to investigate PSMC2-EGFR interactions and downstream signaling. PSMC2 was significantly overexpressed in HCC tissues and correlated with poor patient prognosis. Genetic knockdown of PSMC2 inhibited HCC cell proliferation, migration, and invasion in vitro, while suppressing tumor growth in vivo. Conversely, PSMC2 overexpression enhanced malignant phenotypes. Mechanistically, PSMC2 physically interacted with EGFR, stabilizing EGFR protein levels and enhancing phosphorylation of downstream AKT and ERK1/2 pathways. Our study identifies PSMC2 as a novel regulator of HCC progression through EGFR-AKT/ERK1/2 signaling axis activation. These findings position PSMC2 as both a prognostic biomarker and a potential therapeutic target for HCC intervention.</p>

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PSMC2 promotes hepatocellular carcinoma progression through interaction with EGFR

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月24日

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  • Yecheng Li,
  • Qunxue Su,
  • Zhenyu Feng,
  • Hui Xu,
  • Tengfei He

摘要

Growing evidence highlights the critical involvement of the ubiquitin-proteasome system in cancer development. As an essential component of the 26 S proteasome, Proteasome 26 S Subunit ATPase 2 (PSMC2) has been implicated in various malignancies, but its role in hepatocellular carcinoma (HCC) progression remains poorly understood. We analyzed PSMC2 expression using The Cancer Genome Atlas database (TCGA) database, and validated findings in clinical HCC specimens and cell lines through immunohistochemistry (IHC) and Western blot. Functional assays (CCK-8, colony formation, Scratch test and transwell invasion assay) were performed to assess the oncogenic properties of PSMC2 in the progression of HCC. Mechanistic studies employed co-immunoprecipitation, Western blot, immunofluorescence and in vivo xenograft models to investigate PSMC2-EGFR interactions and downstream signaling. PSMC2 was significantly overexpressed in HCC tissues and correlated with poor patient prognosis. Genetic knockdown of PSMC2 inhibited HCC cell proliferation, migration, and invasion in vitro, while suppressing tumor growth in vivo. Conversely, PSMC2 overexpression enhanced malignant phenotypes. Mechanistically, PSMC2 physically interacted with EGFR, stabilizing EGFR protein levels and enhancing phosphorylation of downstream AKT and ERK1/2 pathways. Our study identifies PSMC2 as a novel regulator of HCC progression through EGFR-AKT/ERK1/2 signaling axis activation. These findings position PSMC2 as both a prognostic biomarker and a potential therapeutic target for HCC intervention.