ArticleWorld journal of surgical oncology2026
Knocking down FAM110A suppresses colon adenocarcinoma progression by inhibiting the Nrf2/HO-1 axis to induce ferroptosis.
Article in World journal of surgical oncology, 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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1 citing paper in PubMed.
- Ellagic Acid Enhances RSL3-Induced Ferroptosis by Inhibiting the Nrf2/HO-1 Signaling Pathway in Pancreatic Ductal Adenocarcinoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
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9 authors.
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Abstract
backgroundThe family with sequence similarity 110 member A (FAM110A) is implicated in cell cycle regulation, but its role in colon adenocarcinoma (COAD) remains unknown. Through integrative bioinformatics analysis, clinical tissue sample validation, and experimental validation, we investigated the role of FAM110A in COAD.
methodsWe employed a comprehensive bioinformatics approach, utilizing The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets, alongside various R packages for data acquisition and analysis. The clinical COAD tissue samples and their corresponding paracancerous normal colonic mucosa samples were collected for immunohistochemical (IHC) staining to verify the expression of FAM110A in clinical specimens. After knocking down FAM110A, the cell viability, migration, invasion, cell cycle, apoptosis, reactive oxygen species (ROS), malondialdehyde (MDA), 4-hydroxynonenoic acid (4-HNE), Fe
resultsMultiple differentially expressed genes in COAD in the TCGA-COAD and GSE20916 datasets were identified. The elevated expression of FAM110A in tumor samples compared to normal tissues suggested its potential diagnostic role in COAD. Multivariate Cox regression models incorporating clinical variables indicated that FAM110A was one of the independent prognostic factors for COAD. The drug sensitivity analysis revealed correlations between FAM110A and the efficacy of several anticancer drugs. Clinical tissue IHC analysis further confirmed the significantly higher expression of FAM110A in COAD tumor tissues compared with paired paracancerous normal colonic mucosa tissues. The immune infiltration analysis revealed that FAM110A could serve as a biomarker for predicting response to immunotherapies for COAD. FAM110A was enriched in multiple pathways. Knocking down FAM110A reduced cell viability, migration, invasion, and GSH levels, as well as GPX4, SLC7A11, Nrf2, and HO-1 protein expression levels, arrested the cell cycle, and elevated apoptosis, ROS, MDA, 4-HNE, and Fe
conclusionsOur findings underscore the diagnostic and prognostic significance of FAM110A in COAD. Knocking down FAM110A alleviated COAD via Nrf2/HO-1 axis inhibition to promote ferroptosis, and Nrf2 overexpression could rescue the ferroptosis and growth inhibition induced by FAM110A deficiency, providing a theoretical basis for developing drugs targeting FAM110A for treating COAD.
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