Authors
Huaqing Yan, Fan Xu, Xiaobo Cui, Sinian Zheng, Dianjun Yu, Yiming Wu, Bangbin Chen, Rubing Li
Published in
Discover oncology. Jul 05, 2026. Epub Jul 05, 2026.
Abstract
FMR1, a gene classically linked to Fragile X syndrome, functions as a multifunctional RNA-binding protein regulating RNA metabolism. Emerging evidence indicates its role in modulating cancer progression and tumor immunity, yet a comprehensive pan-cancer analysis to confirm its viability as a biomarker for cancer screening, prognosis, and precision therapy remains lacking.
We first validated FMR1 expression in renal cell carcinoma cell lines via qRT-PCR and assessed its functional role using colony-formation, wound-healing, and Transwell assays. Subsequently, we performed pan-cancer analyses by mining multi-omic data from public databases including UCSC Xena, TCGA, GTEx, TIMER, and TISIDB, integrating expression, prognosis, immune infiltration, and genetic alteration data.
FMR1 was downregulated in renal cancer cell lines, and its overexpression inhibited cell proliferation and migration. Pan-cancer analysis revealed dysregulated FMR1 expression across multiple tumors. Low FMR1 expression correlated with poor prognosis in cancers like KIRC and SKCM. It also correlated with RNA methylation genes, immune/molecular subtypes, immune checkpoint genes, and immune cell infiltration. FMR1 amplification was the most frequent genetic alteration, and it demonstrated possibly improved predictive value compared to some traditional biomarkers.
FMR1 acts as a tumor suppressor in renal cancer and represents a promising pan-cancer biomarker for screening, prognostic evaluation, and immunotherapy response prediction, providing new insights for precision cancer therapy.
PMID:
42402078
Bibliographic data and abstract were imported from PubMed on 05 Jul 2026.
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