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Original Article

J App Pharm Sci. 2022; 12(11): 157-168

Degalactotigonin induces cytotoxicity and cell cycle arrest in triple negative breast cancer cells (MDA MB 231)

D. Hamsa, K. Swathi, Sri Renukadevi Balusamy, S. Sumathi.

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Triple negative breast cancer (TNBC) is a complicated heterogeneous condition characterized by the lack of three hallmark receptors: human epidermal growth factor receptor 2, estrogen receptor, and progesterone receptor. TNBC is much more lethal than other subtypes of breast cancer, has a greater frequency in African-Americans, and affects younger people more often. The purpose of this study was to explore the cytotoxicity and cell cycle arrest caused by the combination of the compound degalactotigonin and the standard chemotherapeutic agent etoposide in triple negative breast cancer cells (MDA MB 231). In this study, the efficacy of degalactotigonin and etoposide in single and combined forms was evaluated for their ability to modulate cell viability; the extent of DNA damage, metastasis, and apoptosis; and regulation of gene expression in the triple negative breast cancer (MDA MB 231) cell line. The outcomes of this study demonstrated that the combination of degalactotigonin and etoposide had a synergistic impact on triple negative breast cancer cells (MDA MB 231) by suppressing metastatic TNBC cell migration and invasion. The synergic effect of degalactotigonin and etoposide helps to induce cytotoxicity and apoptotic cell death on MDA MB 231. This suggests that the cell death by degalactotigonin could be a promising strategy for cancer therapy.

Key words: Anticancer, Degalactotigonin, Solanum nigrum and Triple Negative Breast Cancer.

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