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In Vitro Apoptotic and Antiproliferative Effects of Propranolol on Human Breast Cancer Cells

dc.authorwosid Terzi, Menderes Yusuf/Z-1999-2018
dc.authorwosid Alizade, Ares/Aba-2470-2021
dc.contributor.author Alizade, Ares
dc.contributor.author Terzi, Menderes Yusuf
dc.date.accessioned 2025-05-10T17:23:00Z
dc.date.available 2025-05-10T17:23:00Z
dc.date.issued 2024
dc.department T.C. Van Yüzüncü Yıl Üniversitesi en_US
dc.department-temp [Alizade, Ares] Van Yuzuncu Yil Univ, Fac Med, Dept Pharmacol, Van, Turkiye; [Terzi, Menderes Yusuf] Hatay Mustafa Kemal Univ, Fac Med, Dept Med Biol, Hatay, Turkiye; [Terzi, Menderes Yusuf] Hatay Mustafa Kemal Univ, Grad Sch Hlth Sci, Dept Mol Biochem & Genet, Hatay, Turkiye en_US
dc.description.abstract Breast cancer is an issue of concern with increasing incidence among women worldwide. Propranolol, as an antihypertensive drug, exerts anticancer effects too. We conducted this study to analyze the in vitro apoptotic and antiproliferative effects of propranolol in human MCF-7 breast cancer cells. MCF-7 cells were seeded into 6 -well plates and treated with 50 mu L propranolol for 24 hours. After cell homogenization, the levels of pro-apoptotic proteins BCL2 associated X (BAX), apoptosis inducing factor (AIF), C/-EBP homologous protein (GADD153), and glucose -regulated protein 78 (GRP78), anti-apoptotic protein BCL2 apoptosis regulator (BCL-2), and cycle -regulator WEE1 G2 checkpoint kinase (WEE1) were measured with ELISA. Propranolol significantly upregulated pro-apoptotic proteins AIF, BAX, GADD153, and GRP78 while downregulated anti-apoptotic protein BCL2. The level of WEE1, as the main regulatory cell cycle protein at the G2/M checkpoint, significantly increased after propranolol treatment. Propranolol inhibited the proliferation of MCF-7 human breast cancer cells by upregulating pro-apoptotic factors AIF, BAX, GADD153 and GRP78 and by downregulating antiapoptotic BCL2. Elevated WEE1 levels after propranolol treatment might lead the tumor cells into a sustained cell -cycle arrest which eventually resulted in caspase-dependent or -independent mitochondrial or endoplasmic-reticulum stress -induced apoptosis. So, propranolol can be utilized as a potential therapeutic agent in breast cancer therapy. en_US
dc.description.sponsorship Hatay Mustafa Kemal University Scientific Research Projects Funding; [18.M.105] en_US
dc.description.sponsorship This project was supported by Hatay Mustafa Kemal University Scientific Research Projects Funding (Project number: 18.M.105). en_US
dc.description.woscitationindex Science Citation Index Expanded
dc.identifier.doi 10.56042/ijeb.v62i05.6304
dc.identifier.endpage 331 en_US
dc.identifier.issn 0019-5189
dc.identifier.issn 0975-1009
dc.identifier.issue 5 en_US
dc.identifier.scopusquality N/A
dc.identifier.startpage 326 en_US
dc.identifier.uri https://doi.org/10.56042/ijeb.v62i05.6304
dc.identifier.uri https://hdl.handle.net/20.500.14720/10757
dc.identifier.volume 62 en_US
dc.identifier.wos WOS:001222087800005
dc.identifier.wosquality Q4
dc.language.iso en en_US
dc.publisher Natl inst Science Communication-niscair en_US
dc.relation.publicationcategory Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı en_US
dc.rights info:eu-repo/semantics/openAccess en_US
dc.subject Anitcancer en_US
dc.subject Antitumorigenic Activity en_US
dc.subject Mcf7 en_US
dc.title In Vitro Apoptotic and Antiproliferative Effects of Propranolol on Human Breast Cancer Cells en_US
dc.type Article en_US

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