4.6 Article

G2/M-Phase-Inhibitory Mitochondrial-Depolarizing Re(I)/Ru(II)/Ir(III)-2,2?-Bipyrimidine-Based Heterobimetallic Luminescent Complexes: An Assessment of In Vitro Antiproliferative Activity and Bioimaging for Targeted Therapy toward Human TNBC Cells

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ACS OMEGA
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AMER CHEMICAL SOC
DOI: 10.1021/acsomega.2c08285

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Triple-negative breast cancer (TNBC) is an extremely aggressive subtype of breast cancer, with the worst prognosis and high invasive and metastatic abilities. Metal complexes have shown anticancer activity and are being studied for their potential in treating breast cancer. New mixed metallic Ru(II)/Ir(III)/Re(I)-2,2'-bipyrimidine complexes [L 'Re2], [L 'RuRe], and [L 'IrRe] were developed to inhibit the uncontrolled proliferation of TNBC cells.
Triple-negative breast cancer (TNBC) is an extremely vicious subtype of human breast cancer having the worst prognosis along with strong invasive and metastatic competency. Hence, it can easily invade into blood vessels, and presently, no targeted therapeutic approach is available to annihilate this type of cancer. Metal complexes have successfully stepped into the anticancer research and are now being applauded due to their anticancer potency after the discovery of cisplatin. Many of these metal complexes are also well recognized for their activity toward breast cancer. As the TNBC is a very dangerous subtype and has long been a challenging ailment to treat, we have intended to develop a few brand new mixed metallic Ru(II)/Ir(III)/ Re(I)-2,2 '-bipyrimidine complexes [L ' Re2], [L ' RuRe], and [L ' IrRe] to abate the unbridled proliferation of TNBC cells. The potency of the complexes against TNBC cells has been justified using MDA-MB-468 TNBC cell lines where complex [L ' IrRe] has displayed significant potency among all the three complexes with an IC50 value of 24.12 mu M. The complex [L ' IrRe] has been competent to cause apoptosis of TNBC cells through inhibition of the G2/M phase in the cell cycle in association with a profuse amount of ROS generation and mitochondrial depolarization.

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