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Peer-reviewedCC BYDiscover Oncology

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

  • Xiang Li1
  • Wei Wang2
  • Ruonan Chai3
  • Changci Tong4
  • Keyang Gong5
5 affiliations
  1. 1Department of Geriatrics, Central Hospital Afffliated to Shenyang Medical College
  2. 2Respiratory and critical care department, the first hospital of China medical university
  3. 3Northern Theater Command General Hospital
  4. 4Shuren International College, Shenyang Medical College
  5. 5Shenyang Medical College
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Abstract

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.

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Cite

BibTeXRIS
BibTeX
@article{li2026fxyd6,
  title = {{FXYD6 functions as a tumor suppressor in lung adenocarcinoma via the OIP5-AS1/miR-4735-3p/FXYD6 axis}},
  author = {Xiang Li and Wei Wang and Ruonan Chai and Changci Tong and Keyang Gong},
  journal = {Discover Oncology},
  year = {2026},
  month = jul,
  doi = {10.1007/s12672-026-05635-4},
  url = {https://doi.org/10.1007/s12672-026-05635-4},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - FXYD6 functions as a tumor suppressor in lung adenocarcinoma via the OIP5-AS1/miR-4735-3p/FXYD6 axis
AU  - Xiang Li
AU  - Wei Wang
AU  - Ruonan Chai
AU  - Changci Tong
AU  - Keyang Gong
PY  - 2026
DA  - 2026/07/01
JO  - Discover Oncology
DO  - 10.1007/s12672-026-05635-4
UR  - https://doi.org/10.1007/s12672-026-05635-4
AB  - 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.
SN  - 2730-6011
ER  -