ArticleMolecular oncology2013
Whole transcriptome analysis of the ERα synthetic fragment P295-T311 (ERα17p) identifies specific ERα-isoform (ERα, ERα36)-dependent and -independent actions in breast cancer cells.
Article in Molecular oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
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- Sex steroid hormone residues in milk and their potential risks for breast and prostate cancer.Frontiers in nutrition · 2024Review
- Promising Perspectives of the Antiproliferative GPER Inverse Agonist ERα17p in Breast Cancer.Cells · 2023Article
- Importins involved in the nuclear transportation of steroid hormone receptors:Frontiers in endocrinology · 2022Article
- The Antitumor Peptide ERα17p Exerts Anti-Hyperalgesic and Anti-Inflammatory Actions Through GPER in Mice.Frontiers in endocrinology · 2021Article
- Article
- The Peptide ERα17p Is a GPER Inverse Agonist that Exerts Antiproliferative Effects in Breast Cancer Cells.Cells · 2019Article
- Natural Anti-Estrogen Receptor Alpha Antibodies Able to Induce Estrogenic Responses in Breast Cancer Cells: Hypotheses Concerning Their Mechanisms of Action and Emergence.International journal of molecular sciences · 2018Review
- BCMA (TNFRSF17) Induces APRIL and BAFF Mediated Breast Cancer Cell Stemness.Frontiers in oncology · 2018Article
- Estrogens regulate life and death in mitochondria.Journal of bioenergetics and biomembranes · 2017Review
- Whole transcriptome analysis of the ERα synthetic fragment P295-T311 (ERα17p) identifies specific ERα-isoform (ERα, ERα36)-dependent and -independent actions in breast cancer cells.Molecular oncology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ERα17p is a peptide corresponding to the sequence P295LMIKRSKKNSLALSLT311 of the estrogen receptor alpha (ERα) and initially found to interfere with ERα-related calmodulin binding. ERα17p was subsequently found to elicit estrogenic responses in E2-deprived ERα-positive breast cancer cells, increasing proliferation and ERE-dependent gene transcription. Surprisingly, in E2-supplemented media, ERα17p-induced apoptosis and modified the actin network, influencing cell motility. Here, we report that ERα17p internalizes in breast cancer cells (T47D, MDA-MB-231, SKBR3) and induces a massive early (3 h) transcriptional activity. Remarkably, about 75% of significantly modified transcripts were also modified by E2, confirming the pro-estrogenic profile of ERα17p. The different ER spectra of the used cell lines allowed us to identify a specific ERα17p signature related to ERα as well as its variant ERα36. With respect to ERα, the peptide activates nuclear (cell cycle, cell proliferation, nucleic acid and protein synthesis) and extranuclear signaling pathways. In contrast, through ERα36, it mainly triggers inhibitory actions on inflammation. This is the first work reporting a detailed ERα36-specific transcriptional signature. In addition, we report that ERα17p-induced transcripts related to apoptosis and actin modifying effects of the peptide are independent from its estrogen receptor(s)-related actions. We discuss our findings in view of the potential use of ERα17p as a selective peptidomimetic estrogen receptor modulator (PERM).
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