ArticleCancer medicine2019
Chlorotoxin targets ERα/VASP signaling pathway to combat breast cancer.
Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Estrogen Receptor Beta Isoforms Interplay Integrates Nuclear and Extra-Nuclear Signaling to Modulate Human Granulosa Cell Growth.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Toxin-Derived Peptides as Potentials Weapons Against Cancer.Pharmaceutics · 2026Review
- Therapeutic Potential of Scorpion Venom Proteins: Innovations in Cancer Treatment and Future Directions.Current drug targets · 2026Review
- Systematic Review of the Antitumor Activities and Mechanisms of Scorpion Venom on Human Breast Cancer Cells Lines (In Vitro Study).Journal of clinical medicine · 2025Review
- Harnessing the potency of scorpion venom-derived proteins: applications in cancer therapy.Bioresources and bioprocessing · 2024Review
- Venom-derived peptides for breaking through the glass ceiling of drug development.Frontiers in chemistry · 2024Review
- Diagnostic and Therapeutic Approaches for Glioblastoma and Neuroblastoma Cancers Using Chlorotoxin Nanoparticles.Cancers · 2023Review
- Review
- Reptiles as Promising Sources of Medicinal Natural Products for Cancer Therapeutic Drugs.Pharmaceutics · 2022Review
- Toxic Animal-Based Medicinal Materials Can Be Effective in Treating Endometriosis: A Scoping Review.Toxins · 2021Article
- Chlorotoxin targets ERα/VASP signaling pathway to combat breast cancer.Cancer medicine · 2019Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is one of the most common malignant tumors among women worldwide. About 70-75% of primary breast cancers belong to estrogen receptor (ER)-positive breast cancer. In the development of ER-positive breast cancer, abnormal activation of the ERα pathway plays an important role and is also a key point leading to the failure of clinical endocrine therapy. In this study, we found that the small molecule peptide chlorotoxin (CTX) can significantly inhibit the proliferation, migration and invasion of breast cancer cells. In in vitro study, CTX inhibits the expression of ERα in breast cancer cells. Further studies showed that CTX can directly bind to ERα and change the protein secondary structure of its LBD domain, thereby inhibiting the ERα signaling pathway. In addition, we also found that vasodilator stimulated phosphoprotein (VASP) is a target gene of ERα signaling pathway, and CTX can inhibit breast cancer cell proliferation, migration, and invasion through ERα/VASP signaling pathway. In in vivo study, CTX significantly inhibits growth of ER overexpressing breast tumor and, more importantly, based on the mechanism of CTX interacting with ERα, we found that CTX can target ER overexpressing breast tumors in vivo. Our study reveals a new mechanism of CTX anti-ER-positive breast cancer, which also provides an important reference for the study of CTX anti-ER-related tumors.
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