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<p>EDIL3 is a secreted extracellular matrix protein implicated in tumor progression; however, its biological function in clear cell renal cell carcinoma (ccRCC) remains poorly defined. In this study, we systematically investigated the expression profile, functional roles, and underlying mechanisms of EDIL3 in ccRCC. We found that EDIL3 was significantly upregulated in ccRCC tissues and cell lines. Functional assays demonstrated that EDIL3 markedly enhanced the proliferative, migratory, and invasive capacities of ccRCC cells. Mechanistically, EDIL3 promoted epithelial–mesenchymal transition (EMT), as evidenced by downregulation of E-cadherin and upregulation of N-cadherin and Vimentin. Further analyses revealed that EDIL3 activated the PI3K/AKT signaling pathway, and sustained activation of this pathway effectively reversed the suppression of EMT and malignant phenotypes induced by EDIL3 depletion.Collectively, our findings identify EDIL3 as a critical regulator of ccRCC cell malignancy by linking extracellular matrix dynamics to PI3K/AKT-driven EMT programs, thereby providing mechanistic insight into its role in ccRCC progression.</p>

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Activation of the PI3K/AKT pathway by EDIL3 induces EMT and promotes tumor progression in clear cell renal cell carcinoma

  • 期刊论文

  • 发表日期：

    2026年3月4日

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  • Lesha Tao,
  • Wei Xie,
  • Yue Du,
  • Ronggui Zhang

摘要

EDIL3 is a secreted extracellular matrix protein implicated in tumor progression; however, its biological function in clear cell renal cell carcinoma (ccRCC) remains poorly defined. In this study, we systematically investigated the expression profile, functional roles, and underlying mechanisms of EDIL3 in ccRCC. We found that EDIL3 was significantly upregulated in ccRCC tissues and cell lines. Functional assays demonstrated that EDIL3 markedly enhanced the proliferative, migratory, and invasive capacities of ccRCC cells. Mechanistically, EDIL3 promoted epithelial–mesenchymal transition (EMT), as evidenced by downregulation of E-cadherin and upregulation of N-cadherin and Vimentin. Further analyses revealed that EDIL3 activated the PI3K/AKT signaling pathway, and sustained activation of this pathway effectively reversed the suppression of EMT and malignant phenotypes induced by EDIL3 depletion.Collectively, our findings identify EDIL3 as a critical regulator of ccRCC cell malignancy by linking extracellular matrix dynamics to PI3K/AKT-driven EMT programs, thereby providing mechanistic insight into its role in ccRCC progression.