Cytotoxicity of SHIP2 Silencing in MDA-MB-231 Breast Cancer Cell Line

Background: Breast cancer is a serious global health risk to women. Compared to other forms of BC. Triple negative breast cancer is characterized by a poor prognosis, high levels of aggressiveness and proliferation, and rapid progression. The phosphoinositide 3-kinase/ protein kinase B/ mechanistic target of rapamycin signaling pathway is commonly over-activated in human cancers and plays a role in BC survival, proliferation and angiogenesis. The SH2-containing 5´ inositol phosphatases 1 and 2, contribute to the regulation of the phosphoinositide 3-kinase/ protein kinase B signaling pathway that has a role in progression of cancer. Objective: To address the cytotoxic effect of SH2-containing 5´ inositol phosphatases 2 silencing in MDA-MB-231 BC cell line. Methods: The MDA-MB-231 cells were cultured in Dulbecco’s modified Eagle’s medium with low glucose, with and without SHIP2- small interfering ribonucleic acid for SH2-containing 5´ inositol phosphatases 2 transfection. The cytotoxicity of SH2-containing 5´ inositol phosphatases 2 silencing was assessed by [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. Apoptosis was assessed using Annexin V-fluorescein isothiocyanate/ propidium iodide staining. Results: Transfection of MDA-MB-231 BC cells with (0.04 µM) of SHIP2-siRNA significantly reduced cell viability at 24 hours post-transfection, and significantly induced apoptosis compared to control untreated cells. Conclusion: The present study provided evidence that SHIP2-siRNA reduced viability and induced apoptosis at 24 hours post-transfection in MDA-MB-231 BC cells.

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Journal
Al Mustansiriyah Journal of Pharmaceutical Sciences
Published
2025-12-31
DOI
https://doi.org/10.32947/ajps.v25i5.1332
Primary Topic
PI3K/AKT/mTOR signaling in cancer
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article
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article

Cytotoxicity of SHIP2 Silencing in MDA-MB-231 Breast Cancer Cell Line

Riyad Naser, Inam Sameh Arif, Basma Talib Al-Sudani, Sayed Mahmood Alqallaf
Al Mustansiriyah Journal of Pharmaceutical Sciences
PI3K/AKT/mTOR signaling in cancer
article

Cytotoxicity of SHIP2 Silencing in MDA-MB-231 Breast Cancer Cell Line

Riyad Naser, Inam Sameh Arif, Basma Talib Al-Sudani, Sayed Mahmood Alqallaf
article en

Abstract

Background: Breast cancer is a serious global health risk to women. Compared to other forms of BC. Triple negative breast cancer is characterized by a poor prognosis, high levels of aggressiveness and proliferation, and rapid progression. The phosphoinositide 3-kinase/ protein kinase B/ mechanistic target of rapamycin signaling pathway is commonly over-activated in human cancers and plays a role in BC survival, proliferation and angiogenesis. The SH2-containing 5´ inositol phosphatases 1 and 2, contribute to the regulation of the phosphoinositide 3-kinase/ protein kinase B signaling pathway that has a role in progression of cancer. Objective: To address the cytotoxic effect of SH2-containing 5´ inositol phosphatases 2 silencing in MDA-MB-231 BC cell line. Methods: The MDA-MB-231 cells were cultured in Dulbecco’s modified Eagle’s medium with low glucose, with and without SHIP2- small interfering ribonucleic acid for SH2-containing 5´ inositol phosphatases 2 transfection. The cytotoxicity of SH2-containing 5´ inositol phosphatases 2 silencing was assessed by [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. Apoptosis was assessed using Annexin V-fluorescein isothiocyanate/ propidium iodide staining. Results: Transfection of MDA-MB-231 BC cells with (0.04 µM) of SHIP2-siRNA significantly reduced cell viability at 24 hours post-transfection, and significantly induced apoptosis compared to control untreated cells. Conclusion: The present study provided evidence that SHIP2-siRNA reduced viability and induced apoptosis at 24 hours post-transfection in MDA-MB-231 BC cells.

Al Mustansiriyah Journal of Pharmaceutical SciencesVol. 25(5)
University of Bahrain (BH), Mustansiriyah University (IQ), University College of Bahrain (BH)
Good health and well-being
Openalex Percentile: Top 35%
PI3K/AKT/mTOR signaling in cancer
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