Abstract
Cisplatin is one of the most effective anticancer agents used to treat colon cancer, which is the third malignancy between the most common human cancers in the world, but the resistance developed represents an obstacle against the full success of chemotherapy. An emerging interest appeared in finding other metallic compounds, such as ruthenium(III) complexes, for chemotherapeutic application in cancer. Our study focused on the anticancer activity of several ruthenium (Ru) complexes with quinolone antibiotics in colon tumor cell cultures. Real-time cell analysis and drug-mediated cytotoxicity tests monitored the inhibitory effects in the drug-treated LoVo colon cancer cells. Flow cytometry assays were performed to evaluate cell cycle phases distribution and apoptotic events. The obtained results showed dose-dependent increased levels of cell lysis and induction of apoptosis in LoVo cancer cells treated with the Ru(III) complexes. In addition, data showed a major decrease in cell proliferation, since the percentages of cells distributed in the S cell cycle phase diminished, and a G0/G1 cell arrest was observed. Therefore, our results strongly suggest that the newly synthesized Ru(III) complexes might play an important role in future chemotherapeutic approaches, since their activity is based on diminishing cell proliferation, induction of apoptosis, and modulation of cell cycle phases.
Highlights
Cancer is a major public health problem worldwide with an estimated 19.3 million new cancer cases and almost 10.0 million cancer deaths occurring in 2020
Changes in a cell status, such as cell morphology, cell adhesion, or cell viability led to a change in cell index (CI), which is a quantitative measure of the cell number present in a well [7,48]
Changes in cell status, such as cell morphology, adhesion, or viability led to a change in cell index (CI), which is a quantitative measure of the cell number present in a well [58]
Summary
Cancer is a major public health problem worldwide with an estimated 19.3 million new cancer cases and almost 10.0 million cancer deaths occurring in 2020. Resistance to chemotherapy and molecularly targeted therapies is a major problem facing current cancer research [8,9], and the number of drugs that have been shown to induce resistance in cancer cell killing is rapidly increasing, possibly through the modulation of survival cell components, such as proliferative or anti-apoptotic proteins [10,11,12]. The mechanisms of resistance to “classical” cytotoxic chemotherapeutics and to therapies that are designed to be selective for specific molecular targets share many features, such as alterations in the drug target, activation of pro-survival pathways, and ineffective induction of cell death [13,14,15]
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