ArticleJournal of proteome research2024
Proteomic Analysis Reveals Major Proteins and Pathways That Mediate the Effect of 17-β-Estradiol in Cell Division and Apoptosis in Breast Cancer MCF7 Cells.
Article in Journal of proteome research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Differential Effects of 17β-Estradiol, Its Metabolites, and Cadmium on Cytotoxicity and Redox-Related Pathways in Doxorubicin-Sensitive and -Resistant Breast Cancer Cell Lines.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Polycyclic aromatic hydrocarbon derivative 3-hydroxybenz[a]anthracene promotes the progression of T47D breast cancer cells by modulating relevant protein expression.Frontiers in cell and developmental biology · 2026Article
- Effect of Ipomoeassin F on the Synthesis of Membrane and Secretory Proteins in Triple-Negative Breast Cancer Cells.ACS omega · 2025Article
- Untargeted metabolomics reveals stage-specific metabolic signatures in yak colostrum, transitional milk and mature milk.Food chemistry: X · 2025Article
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Authors and funding
4 authors.
Funding
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Abstract
Despite extensive research, the genes/proteins and pathways responsible for the physiological effects of estrogen remain elusive. In this study, we determined the effect of estrogen on global protein expression in breast cancer MCF7 cells using a proteomic method. The expression of 77 cytosolic, 74 nuclear, and 81 membrane/organelle proteins was significantly altered by 17-β-estradiol (E2). Protein enrichment analyses suggest that E2 may stimulate cell division primarily by promoting the G1 to S phase transition and advancing the G2/M checkpoint. The effect of E2 on cell survival was complex, as it could simultaneously enhance and inhibit apoptosis. Bioinformatics analysis suggests that E2 may enhance apoptosis by promoting the accumulation of the pore-forming protein Bax in the mitochondria and inhibit apoptosis by activating the PI3K/AKT/mTOR signaling pathway. We verified the activation of the PI3K signaling and the accumulation of Bax in the membrane/organelle fraction in E2-treated cells using immunoblotting. Treatment of MCF7 cells with E2 and the PI3K inhibitor Ly294002 significantly enhanced apoptosis compared to those treated with E2 alone, suggesting that combining estrogen with a PI3K inhibitor could be a promising strategy for treating ERα-positive breast cancer. Interestingly, many of the E2-upregulated proteins contained the HEAT, KH, and RRM domains.
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