ArticleOncogene2022
Aberrant promoter hypermethylation inhibits RGMA expression and contributes to tumor progression in breast cancer.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 27 citations in OpenAlex.
- Ketogenic diet can inhibit epileptic seizures by inhibiting RGMa methylation to promote GluA1 palmitoylation in the epileptic rat model.Nutrition & metabolism · 2026Article
- Integration of scRNA-seq and bulk tissue RNA-seq data to identify cancer-associated fibroblast-related gene RGMA as a potential treatment target for esophageal cancer.Functional & integrative genomics · 2025Article
- Therapeutic Targets for Gastric Cancer: Mendelian Randomization and Colocalization Analysis.Biological procedures online · 2025Article
- Heterogeneous Clustering of Multiomics Data for Breast Cancer Subgroup Classification and Detection.International journal of molecular sciences · 2025Article
- Epigenetic crosstalk between stem cells and tumors: mechanisms and emerging perspectives.American journal of stem cells · 2025Review
- Expression, DNA methylation pattern and transcription factor EPB41L3 in gastric cancer: a study of 262 cases.Cell communication and signaling : CCS · 2024Article
- Transfection with Plasmid-Encoding lncRNA-SLERCC nanoparticle-mediated delivery suppressed tumor progression in renal cell carcinoma.Journal of experimental & clinical cancer research : CR · 2022Article
- LncRNA RP11-551L14.4 suppresses breast cancer development by inhibiting the expression of miR-4472.PeerJ · 2022Article
- Association betweenPeerJ · 2022Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
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Abstract
Breast cancer (BC) is the most common cancer in women worldwide, and the exploration of aberrantly expressed genes might clarify tumorigenesis and help uncover new therapeutic strategies for BC. Although RGMA was recently recognized as a tumor suppressor gene, its detailed biological function and regulation in BC remain unclear. Herein, we found that RGMA was downregulated in BC tissues compared with non-tumorous breast tissues, particularly in metastatic BC samples, and that patients with low RGMA expression manifested a poorer prognosis. Furthermore, DNMT1 and DNMT3A were found to be recruited to the RGMA promoter and induced aberrant hypermethylation, resulting in downregulation of RGMA expression in BC. In contrast, RGMA overexpression suppressed BC cell proliferation and colony-formation capabilities and increased BC cell apoptosis. Furthermore, RGMA knockdown accelerated BC cell proliferation and suppressed cellular apoptosis in vitro and in vivo. Reversal of RGMA promoter methylation with 5-Aza-CdR restored RGMA expression and blocked tumor growth. Overall, DNMT1- and DNMT3A-mediated RGMA promoter hypermethylation led to downregulation of RGMA expression, and low RGMA expression contributed to BC growth via activation of the FAK/Src/PI3K/AKT-signaling pathway. Our data thus suggested that RGMA might be a promising therapeutic target in BC.
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