ArticleMolecular & cellular proteomics : MCP2024
Proteomic Analysis Revealed the Potential Role of MAGE-D2 in the Therapeutic Targeting of Triple-Negative Breast Cancer.
Article in Molecular & cellular proteomics : MCP, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Monoallelic expression characterizes a distinct molecular and clinical group of breast tumors.Research square · 2026Article
- Cross-Species Upregulation ofCurrent issues in molecular biology · 2026Article
- Targeting the MAGED2-TRIM28-FLNC axis overcomes chemoresistance in TNBC via EMT suppression.Cell communication and signaling : CCS · 2025Article
- Proteomics in Diagnostic Evaluation and Treatment of Breast Cancer: A Scoping Review.Journal of personalized medicine · 2025Review
- Systematic proteomics analysis revealed different expression of laminin interaction proteins in breast cancer: lower in luminal subtype and higher in claudin-low subtype.Translational cancer research · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
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Abstract
Among all the molecular subtypes of breast cancer, triple-negative breast cancer (TNBC) is the most aggressive one. Currently, the clinical prognosis of TNBC is poor because there is still no effective therapeutic target. Here, we carried out a combined proteomic analysis involving bioinformatic analysis of the proteome database, label-free quantitative proteomics, and immunoprecipitation (IP) coupled with mass spectrometry (MS) to explore potential therapeutic targets for TNBC. The results of bioinformatic analysis showed an overexpression of MAGE-D2 (melanoma antigen family D2) in TNBC. In vivo and in vitro experiments revealed that MAGE-D2 overexpression could promote cell proliferation and metastasis. Furthermore, label-free quantitative proteomics revealed that MAGE-D2 acted as a cancer-promoting factor by activating the PI3K-AKT pathway. Moreover, the outcomes of IP-MS and cross-linking IP-MS demonstrated that MAGE-D2 could interact with Hsp70 and prevent Hsp70 degradation, but evidence for their direct interaction is still lacking. Nevertheless, MAGE-D2 is a potential therapeutic target for TNBC, and blocking MAGE-D2 may have important therapeutic implications.
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