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<p>Glutathione peroxidase 7 (GPX7) has been implicated in tumorigenesis and cancer progression across various malignancies. However, its functional role and clinical significance in hepatocellular carcinoma (HCC) remain poorly understood. The expression profile of GPX7 in HCC was analyzed using data from TCGA, GEO, and ICGC. Kaplan-Meier survival curves and receiver operating characteristic curve analysis were used to assess the prognostic and diagnostic value of GPX7. The drug sensitivity of GPX7 and functional enrichment analysis were investigated in the TCGA database. qRT-PCR, IHC, and WB validated the expression of GPX7 in HCC. CCK-8/EdU assayed to detect the effect of GPX7 on HCC proliferation and transwell assayed to detect the effect of GPX7 on HCC migration and invasion. Our analysis showed that GPX7 was upregulated in HCC normal counterparts. Elevated GPX7 was associated with decreased overall survival and increased diagnostic accuracy, as well as shown to correlate with chemoresistance in the TCGA database. Cell proliferation and metastasis were significantly inhibited by knockdown of GPX7 in HCC cell lines. Mechanistically, functional enrichment analysis and WB revealed that GPX7 overexpression could activate the PI3K/AKT pathway and epithelial-mesenchymal transition (EMT) to promote tumor progression. This study identifies GPX7 as a relevant oncogenic driver in HCC pathogenesis through PI3K-AKT/EMT axis activation. The strong diagnostic properties and chemoresistance modulation make GPX7 a promising therapeutic biomarker for the treatment of HCC.</p>

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GPX7 Accelerates epithelial-mesenchymal Transition and Drives HCC Progression Via PI3K/AKT Signaling Pathway

  • 期刊论文

  • 发表日期：

    2025年10月10日

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  • Cangyuan Zhang,
  • Likai Gu,
  • Yi Zhou,
  • Xihu Qin,
  • Chen Xiong

摘要

Glutathione peroxidase 7 (GPX7) has been implicated in tumorigenesis and cancer progression across various malignancies. However, its functional role and clinical significance in hepatocellular carcinoma (HCC) remain poorly understood. The expression profile of GPX7 in HCC was analyzed using data from TCGA, GEO, and ICGC. Kaplan-Meier survival curves and receiver operating characteristic curve analysis were used to assess the prognostic and diagnostic value of GPX7. The drug sensitivity of GPX7 and functional enrichment analysis were investigated in the TCGA database. qRT-PCR, IHC, and WB validated the expression of GPX7 in HCC. CCK-8/EdU assayed to detect the effect of GPX7 on HCC proliferation and transwell assayed to detect the effect of GPX7 on HCC migration and invasion. Our analysis showed that GPX7 was upregulated in HCC normal counterparts. Elevated GPX7 was associated with decreased overall survival and increased diagnostic accuracy, as well as shown to correlate with chemoresistance in the TCGA database. Cell proliferation and metastasis were significantly inhibited by knockdown of GPX7 in HCC cell lines. Mechanistically, functional enrichment analysis and WB revealed that GPX7 overexpression could activate the PI3K/AKT pathway and epithelial-mesenchymal transition (EMT) to promote tumor progression. This study identifies GPX7 as a relevant oncogenic driver in HCC pathogenesis through PI3K-AKT/EMT axis activation. The strong diagnostic properties and chemoresistance modulation make GPX7 a promising therapeutic biomarker for the treatment of HCC.