Maryam Dehdashti Young Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran Zahra Abbasy Faculty of Medicine, Kashan University of Medical Sciences, Kashan, Iran Hamid Zaferani Arani Department of Surgery, Shariati Hospital. Tehran University of Medical Sciences, Tehran, Iran Hesam Adin Atashi Young Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran Seyed Alireza Salimi-Tabatabaee Department of Surgery, Kashan University of Medical Sciences, Kashan, Iran Afsaneh Ghasemi Department of Public Health, School of Health, Fasa University of Medical Sciences, Fasa, Iran Zhila Fereidouni Department of Nursing, School of Nursing, Fasa University of Medical Sciences, Fasa, Iran Hadi Zare Marzouni Qaen school of Nursing and Midwifery, Birjand University of Medical Sciences, Birjand, Iran Habib Zakeri Research Center for Neuromodulation and Pain, NAB Pain Clinic, Shiraz University of Medical Sciences, Shiraz, Iran https://orcid.org/0000-0003-2495-8507 Seyed Abbas Mirmalek Department of Surgery, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran

Keywords: Vanadyl Sulfate, Breast Cancer, Anti-cancer, MCF-7, Apoptosis, Anti-oxidative

Abstract Background: Breast cancer (BC) is the major cause of death from cancer among women. Some studies have indicated the cytotoxic effects of vanadyl oxide sulfate (VOSO4). This study aimed to evaluate the anti-cancer effect of VOSO4 in the treatment of MCF-7 cell line. Materials and Method: The MCF-7 cell line was treated with different concentrations of VOSO4 for 24 and 48 hours. The measurement of cell death was performed by MTT assay. The cell apoptosis rate was measured using Annexin V/Propidium Iodide assay through flow cytometry. Also, the expression levels of p53, P21, Caspase8, superoxide dismutase type 1 (SOD1), Sod2, and Bcl2 mRNAs were evaluated, and Western blotting was performed for Sod1 protein. Results: The results showed that the half-maximal inhibitory concentration (IC50) for VOSO4 was 25 and 20 μg/ml for 24 and 48 hours, respectively. Indeed, VOSO4 has dose-dependent cytotoxic effects on the MCF-7. Also, the apoptosis of the cells after 24 hours of exposure to VOSO4 reached 52% compared with untreated cells. Moreover, after 24 hours of exposure to VOSO4 with IC50 concentration, the expression of p53, P21, Caspase8, Sod1, and Sod2 mRNAs increased (P<0.05), and the expression of Bcl2 mRNA was decreased (P<0.05). Also, the Western blotting revealed Sod1 protein level markedly increased following exposure to VOSO4 (P<0.05). Conclusion: Our results demonstrated that VOSO4 has an apoptotic and cytotoxic effect on BC cells. Therefore, it could be considered as a complementary agent for the medical treatment of patients with BC.

How to Cite

Dehdashti, M., Abbasy, Z., Zaferani Arani, H., Atashi, H. A., Salimi-Tabatabaee, S. A., Ghasemi, A., Fereidouni, Z., Zare Marzouni, H., Zakeri, H., & Mirmalek, S. A. (2023). Cytotoxic and Apoptotic Effects of Vanadyl Sulfate on MCF-7 Breast Cancer Cell Line. Galen Medical Journal, 12, e3050. https://doi.org/10.31661/gmj.v12i.3050

Copyright (c) 2023 Galen Medical Journal

This work is licensed under a Creative Commons Attribution 4.0 International License.

Authors who publish with this journal agree to the following terms:

Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution 4.0 International License that allows others to share the work with an acknowledgment of the work's authorship and initial publication in this journal. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgment of its initial publication in this journal. Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).