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<p>Lung adenocarcinoma (LUAD) remains a leading cause of cancer mortality. This study identifies FXYD6 as a novel tumor suppressor in LUAD, where it is significantly downregulated. High FXYD6 expression correlates with improved patient survival, and its overexpression inhibits LUAD cell proliferation and migration. Mechanistically, FXYD6 is directly targeted and suppressed by the oncomiR miR-4735-3p, which is upregulated in LUAD. Inhibiting miR-4735-3p elevates FXYD6 levels and suppresses malignant phenotypes. Furthermore, we delineate a complete competing endogenous RNA (ceRNA) axis: the long non-coding RNA OIP5-AS1, which is downregulated in LUAD, functions as a molecular sponge for miR-4735-3p. Overexpression of OIP5-AS1 sequesters miR-4735-3p, thereby derepressing FXYD6 expression and inhibiting cancer progression. Rescue assays confirm that miR-4735-3p overexpression reverses the tumor-suppressive effects of OIP5-AS1. In vivo xenograft models validate that the OIP5-AS1/miR-4735-3p/FXYD6 axis critically regulates tumor growth. Our findings reveal a crucial tumor-suppressive pathway in LUAD, highlighting the long noncoding RNA (lncRNA) OIP5-AS1 as a key upstream regulator that modulates FXYD6 by competitively binding miR-4735-3p. This axis presents a promising therapeutic target for LUAD intervention.</p>

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FXYD6 functions as a tumor suppressor in lung adenocarcinoma via the OIP5-AS1/miR-4735-3p/FXYD6 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月27日

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  • Xiang Li,
  • Wei Wang,
  • Ruonan Chai,
  • Changci Tong,
  • Keyang Gong

摘要

Lung adenocarcinoma (LUAD) remains a leading cause of cancer mortality. This study identifies FXYD6 as a novel tumor suppressor in LUAD, where it is significantly downregulated. High FXYD6 expression correlates with improved patient survival, and its overexpression inhibits LUAD cell proliferation and migration. Mechanistically, FXYD6 is directly targeted and suppressed by the oncomiR miR-4735-3p, which is upregulated in LUAD. Inhibiting miR-4735-3p elevates FXYD6 levels and suppresses malignant phenotypes. Furthermore, we delineate a complete competing endogenous RNA (ceRNA) axis: the long non-coding RNA OIP5-AS1, which is downregulated in LUAD, functions as a molecular sponge for miR-4735-3p. Overexpression of OIP5-AS1 sequesters miR-4735-3p, thereby derepressing FXYD6 expression and inhibiting cancer progression. Rescue assays confirm that miR-4735-3p overexpression reverses the tumor-suppressive effects of OIP5-AS1. In vivo xenograft models validate that the OIP5-AS1/miR-4735-3p/FXYD6 axis critically regulates tumor growth. Our findings reveal a crucial tumor-suppressive pathway in LUAD, highlighting the long noncoding RNA (lncRNA) OIP5-AS1 as a key upstream regulator that modulates FXYD6 by competitively binding miR-4735-3p. This axis presents a promising therapeutic target for LUAD intervention.