---
title: "Vasopressin enhances dynasore and wortmannin antiproliferative effects in triple-negative breast c"
id: "pubmed-42667529"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42667529"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42667529/"
doi: "10.1007/s12032-026-03368-6"
published_at: "2026-08-29T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Vasopressin enhances dynasore and wortmannin antiproliferative effects in triple-negative breast c
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42667529
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42667529/)
- **DOI:** [10.1007/s12032-026-03368-6](https://doi.org/10.1007%2Fs12032-026-03368-6)
- **Published At:** 2026-08-29T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The study investigated the effect of arginine **vasopressin (AVP)** on proliferation of the triple-negative breast cancer cell line **MDA-MB-231**, which expresses the V1A receptor. - Cells were exposed to **100 nM AVP** for 24 hours, alone or combined with the dynamin-2 GTPase inhibitor **Dynasore (DYN)**; parallel experiments used the **PI3K inhibitor wortmannin (Wort)** alone or with DYN. - AVP alone induced apoptosis in approximately **20%** of cells; AVP plus DYN increased apoptosis to **28%**. - Wortmannin alone induced apoptosis in **29%** of cells; Wort+ DYN increased apoptosis to **35%**, indicating additive or synergistic antiproliferative effects when combined with dynamin inhibition. - Apoptosis with treatments correlated with upregulation of **Bax** and **Caspase-3** and cell cycle arrest in **G0/G1** phase. - Cell migration and invasion were reduced with AVP and with combined treatments. - Autophagy markers **LC3II** protein and **Beclin1 mRNA** increased in AVP and AVP+DYN treatments but decreased with Wort and Wort+DYN, indicating divergent autophagy effects dependent on pathway targeted. - Dual treatments (AVP+DYN and Wort+DYN) decreased **AKT** activation and downregulated the multidrug resistance gene **MDR1**. - The authors conclude AVP can induce apoptosis and autophagy-related cell death in invasive breast cancer cells and potentiates the antiproliferative activity of dynamin inhibition; wortmannin shows similar potentiation with DYN. - Ethical approval for the study was obtained (Faculty of Science, Tanta University; Approval code: 3425/11/20).
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Cell Molecular Biology Unit, Division of Biochemistry, Department of Chemistry, Faculty of Science, Tanta University, Tanta, 31527, Egypt. samar.alkafas@science.tanta.edu.eg. * 2 Cell Molecular Biology Unit, Division of Biochemistry, Department of Chemistry, Faculty of Science, Tanta University, Tanta, 31527, Egypt. * 3 Virology & immunology unit Cancer biology Department, National Cancer Institute, Cairo University, Cairo, 11796, Egypt. * 4 Cell Molecular Biology Unit, Division of Biochemistry, Department of Chemistry, Faculty of Science, Tanta University, Tanta, 31527, Egypt. mohamed.hussien1@science.tanta.edu.eg. * PMID: **42667529** * DOI: [ 10.1007/s12032-026-03368-6 ](https://doi.org/10.1007/s12032-026-03368-6) Item in Clipboard # Vasopressin boosts the antiproliferative effect of dynasore and wortmannin in triple-negative breast cancer cells Samar Sami AlKafaas et al. Med Oncol. 2026. Show details Display options Display options Format Abstract PubMed PMID Med Oncol Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Med+Oncol%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Med+Oncol%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) . 2026 Aug 29;43(10):263. doi: 10.1007/s12032-026-03368-6. ### Authors [Samar Sami AlKafaas](https://pubmed.ncbi.nlm.nih.gov/?term=AlKafaas+SS&cauthor_id=42667529)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42667529/#short-view-affiliation-1 "Cell Molecular Biology Unit, Division of Biochemistry, Department of Chemistry, Faculty of Science, Tanta University, Tanta, 31527, Egypt. samar.alkafas@science.tanta.edu.eg."), [Thoria Diab](https://pubmed.ncbi.nlm.nih.gov/?term=Diab+T&cauthor_id=42667529)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42667529/#short-view-affiliation-2 "Cell Molecular Biology Unit, Division of Biochemistry, Department of Chemistry, Faculty of Science, Tanta University, Tanta, 31527, Egypt."), [Samah A Loutfy](https://pubmed.ncbi.nlm.nih.gov/?term=Loutfy+SA&cauthor_id=42667529)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42667529/#short-view-affiliation-3 "Virology & immunology unit Cancer biology Department, National Cancer Institute, Cairo University, Cairo, 11796, Egypt."), [Mohamed Hessien](https://pubmed.ncbi.nlm.nih.gov/?term=Hessien+M&cauthor_id=42667529)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42667529/#short-view-affiliation-4 "Cell Molecular Biology Unit, Division of Biochemistry, Department of Chemistry, Faculty of Science, Tanta University, Tanta, 31527, Egypt. mohamed.hussien1@science.tanta.edu.eg.") ### Affiliations * 1 Cell Molecular Biology Unit, Division of Biochemistry, Department of Chemistry, Faculty of Science, Tanta University, Tanta, 31527, Egypt. samar.alkafas@science.tanta.edu.eg. * 2 Cell Molecular Biology Unit, Division of Biochemistry, Department of Chemistry, Faculty of Science, Tanta University, Tanta, 31527, Egypt. * 3 Virology & immunology unit Cancer biology Department, National Cancer Institute, Cairo University, Cairo, 11796, Egypt. * 4 Cell Molecular Biology Unit, Division of Biochemistry, Department of Chemistry, Faculty of Science, Tanta University, Tanta, 31527, Egypt. mohamed.hussien1@science.tanta.edu.eg. * PMID: **42667529** * DOI: [ 10.1007/s12032-026-03368-6 ](https://doi.org/10.1007/s12032-026-03368-6) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Arginine vasopressin hormone (AVP) is ectopically expressed in breast cancer. Also, in intestinal epithelial and mesangial cells, for example, it acts as a growth-promoting factor when it binds to the GPCR receptor and triggers multiple downstream mitogenic signalling pathways leading to cell proliferation. As Dynamin 2 GTPase (Dyn2) is an integral protein involved in membrane receptor endocytosis, it is unclear how far AVP and Dynasore (DYN), a selective Dyn2 GTPase inhibitor, can modulate the proliferation of invasive breast cancer cells. To explore this, triple-negative breast cancer cells (MDA MB-231), which express V1A, were exposed to 100 nM AVP for 24 h, either alone or in combination with DYN. The cytotoxic effect, apoptosis, and autophagy-mediated cell death were assessed and compared to untreated cells and cells in which the PI3K/AKT pathway was inhibited by wortmannin (Wort). Also, cell cycle progression, migration, and the expression of the drug-resistance gene were investigated. We found that AVP alone developed apoptosis in about 20% of cells, and in the presence of DYN, apoptosis increased to 28%. This was associated with overexpression of Bax and Caspase-3, cell cycle arrest in G0/G1 phase, and regression of cell migration and invasion. In parallel, wortmannin alone or in combination with DYN induced apoptosis in 29% and 35% of cells, respectively. The autophagy markers (the microtubule-associated protein (LC3II) and Beclin1 mRNA) increased in AVP and AVP+DYN-treated cells but decreased in Wort and Wort+DYN-treated cells. Mechanistically, dual treatments (AVP+DYN or Wort+DYN) decreased the AKT activation and downregulated the multidrug resistance gene (MDR1). These findings suggest that AVP demonstrates apoptosis- and autophagy-related cell death and exerts a synergistic antiproliferative effect with DYN against invasive breast cancer cells. **Keywords:** AVP; Dynamin2; Dynasore; Invasive breast cancer; Triple-negative; Wortmannin. © 2026. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declarations. Competing interests: The authors declare that they have no competing interests. Ethics approval: The protocol of the current study was approved by the ethical committee of the Faculty of Science, Tanta University (Approval code: 3425/11/20). Consent to participate: Not applicable. Consent for publication: Not applicable. ## References 1. 1. Organization WH: Fact. Sheet Datail of Breast Cancer. 2014. Available online: . Accessed on 22 June 2021. 2. 1. North WG, Fay MJ, Du J. All three vasopressin receptor sub-types are expressed by small-cell carcinoma. In: Vasopressin and oxytocin: molecular, cellular, and clinical advances. 1998. p. 335–8. - [DOI](https://doi.org/10.1007/978-1-4615-4871-3_42) 3. 1. Glavaš M, Gitlin-Domagalska A, Dębowski D, Ptaszyńska N, Łęgowska A, Rolka K. Vasopressin and its analogues: from natural hormones to multitasking peptides. Int J Mol Sci. 2022;23(6):3068. - [DOI](https://doi.org/10.3390/ijms23063068) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/35328489/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/8955888/) 4. 1. Keegan BP, Akerman BL, Péqueux C, North WG. Provasopressin expression by breast cancer cells: implications for growth and novel treatment strategies. Breast Cancer Res Treat. 2006;95:265–77. - [DOI](https://doi.org/10.1007/s10549-005-9024-8) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/16331351/) 5. 1. Taylor A, Ang V, Jenkins J, Silverlight J, Coombes R, Luqmani Y. Interaction of vasopressin and oxytocin with human breast carcinoma cells. Can Res. 1990;50(24):7882–6. Show all 39 references ## MeSH terms * Androstadienes* / pharmacology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Androstadienes%2Fpharmacology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Androstadienes) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Apoptosis / drug effects Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Apoptosis%2Fdrug+effects%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Apoptosis) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Autophagy / drug effects Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Autophagy%2Fdrug+effects%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Autophagy) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Cell Line, Tumor Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Line%2C+Tumor%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Line%2C+Tumor) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Cell Movement / drug effects Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Movement%2Fdrug+effects%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Movement) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Cell Proliferation* / drug effects Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Proliferation%2Fdrug+effects%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Proliferation) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Female Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Female%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Female) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Humans Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Humans%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Humans) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * MDA-MB-231 Cells Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22MDA-MB-231+Cells%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=MDA-MB-231+Cells) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Signal Transduction / drug effects Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Signal+Transduction%2Fdrug+effects%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Signal+Transduction) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Triple Negative Breast Neoplasms* / drug therapy Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Triple+Negative+Breast+Neoplasms%2Fdrug+therapy%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Triple+Negative+Breast+Neoplasms) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Triple Negative Breast Neoplasms* / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Triple+Negative+Breast+Neoplasms%2Fmetabolism%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Triple+Negative+Breast+Neoplasms) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Triple Negative Breast Neoplasms* / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Triple+Negative+Breast+Neoplasms%2Fpathology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Triple+Negative+Breast+Neoplasms) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Vasopressins* / pharmacology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Vasopressins%2Fpharmacology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Vasopressins) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) * Wortmannin / pharmacology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Wortmannin%2Fpharmacology%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Wortmannin) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42667529/) ## Substances * Wortmannin Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Wortmannin%22%5Bnm%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=%22Wortmannin%22) * [ Add to Search ](https://pubmed.ncbi
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