4-Methylthiazole triggers apoptosis and mitochondrial disruption in HL-60 cells

• Published in: Molecular biology reports 2024-12, Vol.51 (1), p.997-997, Article 997
• Main Authors: Meriç, Neslihan, Kar, Ezgi, Kar, Fatih
• Format: Article
• Language: English
• Subjects: Animal Anatomy; Animal Biochemistry; Annexin V; Antineoplastic Agents - pharmacology; Apoptosis; Apoptosis - drug effects; Biomedical and Life Sciences; Caspase 3 - metabolism; Caspase-3; CD123 antigen; CD45 antigen; Cell signaling; Cell Survival - drug effects; Cell viability; Cytochrome c; Cytochromes c - metabolism; Cytotoxicity; dose response; Flow cytometry; Free radicals; Histology; HL-60 Cells; Humans; immunosuppression; Inflammation; interleukin-10; interleukin-6; Leukemia; Leukemia - drug therapy; Leukemia - metabolism; Leukemia - pathology; Life Sciences; Medical research; Membrane potential; Membrane Potential, Mitochondrial - drug effects; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; mitochondrial membrane; Morphology; neoplasm cells; Original Article; Oxidative stress; Oxidative Stress - drug effects; phenotype; propidium; Propidium iodide; Reactive Oxygen Species - metabolism; Signal Transduction - drug effects; Surface markers; therapeutics; thiazoles; Thiazoles - pharmacology; Tumor microenvironment; Tumor necrosis factor-α; Tumors
• ISSN: 0301-4851; 1573-4978; 1573-4978
• DOI: 10.1007/s11033-024-09939-y

Background Thiazole derivatives are gaining prominence in cancer research due to their potent anti-cancer effects and multifaceted biological activities. In leukemia research, these compounds are particularly studied for their ability to induce apoptosis, disrupt mitochondrial membrane potential (MMP), and modulate cell signaling pathways. Methods and results This study investigates the efficacy of 4-Methylthiazole in inducing apoptosis in HL-60 leukemia cells. Apoptosis was quantified via flow cytometry using FITC Annexin V and propidium iodide staining. Mitochondrial disruption was evaluated through alterations in mitochondrial membrane potential (MMP) as measured by the JC-1 assay. The compound significantly disrupted MMP, activated Caspase-3, and induced the release of Cytochrome C, all of which are critical markers of apoptosis (***p