ArticleCellular and molecular life sciences : CMLS2026
NCOA7 promotes OSCC progression by inhibiting ROS-regulated ferroptosis.
Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
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8 authors.
Funding
Abstract
backgroundOral squamous cell carcinoma (OSCC) is the commonest invasive malignancy in the head and neck regions, with a worse prognosis. Recent studies revealed the role of nuclear receptor coactivator 7 (NCOA7) in promoting tumorigenesis. However, the molecular mechanism remains unclear.
methodsHuman OSCC tissues were collected and stained with H&E and NCOA7. The expression of NCOA7 in both normal and tumor tissues was compared, along with a correlation analysis with clinicopathological parameters. In vitro, NCOA7 was knocked down, and the proliferation, migration, invasion, and ferroptosis were evaluated using CCK-8, transwell and 3D spheroid migration and invasion assays, qRT-PCR, western blot, and immunocytochemistry. The effects of NCOA7 on intracellular reactive oxygen species (ROS) and ferroptosis in OSCC cells were investigated under the treatment of antioxidants N-Acetyl-L-cysteine (NAC), ferroptosis inhibitors deferoxamine mesylate (DFO) and ferrostatin-1 (Fer-1), and ferroptosis inducers erastin. The Institutional Ethics Committee approved all clinical protocols.
resultsSignificantly high expression of NCOA7 was found in OSCC tissues and was linked to the advancement of OSCC. In vitro, NCOA7 knockdown statistically reduced the proliferation, migration, and invasion of OSCC cells, which could be rescued using NAC or Fer-1. Moreover, NCOA7 knockdown cells exhibited significantly high levels of ROS and ferroptosis, which could be reversed using NAC or DFO or Fer-1. Further investigations revealed that inhibiting ROS in OSCC cells reduced ferroptosis, while erastin could reverse its inhibitory effect.
conclusionsNCOA7 promotes OSCC progression by inhibiting ferroptosis through ROS signaling. NCOA7 might be a new therapeutic target for OSCC.
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