Series of Organotin(IV) Compounds with Different Dithiocarbamate Ligands Induced Cytotoxicity, Apoptosis and Cell Cycle Arrest on Jurkat E6.1, T Acute Lymphoblastic Leukemia Cells

• Published in: Molecules (Basel, Switzerland) Switzerland), 2023-04, Vol.28 (8), p.3376
• Main Authors: Rasli, Nur Rasyiqin, Hamid, Asmah, Awang, Normah, Kamaludin, Nurul Farahana
• Format: Article
• Language: English
• Subjects: Acute lymphoblastic leukemia; Acute lymphocytic leukemia; Annexin V; Antineoplastic Agents - pharmacology; Apoptosis; B cells; Bone marrow; Cancer; Cancer therapies; Cell cycle; cell cycle arrest; Cell Cycle Checkpoints; Cell death; Cell Line, Tumor; Chemotherapy; childhood leukemia; Cisplatin; Cytotoxicity; dithiocarbamate; Humans; Jurkat Cells; Leukemia; Lymphatic leukemia; Metal complexes; Organotin Compounds - pharmacology; organotin(IV); Precursor Cell Lymphoblastic Leukemia-Lymphoma; Ribonuclease; Staining; Tin compounds; Vincristine
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules28083376

The discovery of cisplatin has influenced scientists to study the anticancer properties of other metal complexes. Organotin(IV) dithiocarbamate compounds are gaining attention as anticancer agents due to their potent cytotoxic properties on cancer cells. In this study, a series of organotin compounds were assessed for their toxic effects on the Jurkat E6.1 cell line. WST-1 assay was used to determine the cytotoxic effect of the compounds and showed that six out of seven organotin(IV) dithiocarbamate compounds exhibited potent cytotoxic effects toward T-lymphoblastic leukemia cells, Jurkat E6.1 with the concentration of IC ranging from 0.67-0.94 µM. The apoptosis assay by Annexin V-FITC/PI staining showed that all tested compounds induced cell death mainly via apoptosis. Cell cycle analysis assessed using RNase/PI staining showed that organotin(IV) dithiocarbamate compounds induced cell cycle arrest at different phases. In conclusion, the tested organotin(IV) dithiocarbamate compounds demonstrated potent cytotoxicity against Jurkat E6.1 cells via apoptosis and cell cycle arrest at low IC value. However, further studies on the mechanisms of action are required to probe the possible potential of these compounds on leukemia cells before they can be developed into anti-leukemic agents.