Suppressive Effects of Anisomycin on the Proliferation of B16 Mouse Melanoma Cells In Vitro

• Published in: Anticancer research Vol. 41; no. 12; pp. 6113 - 6121
• Main Authors: Ushijima, Hironori, Monzaki, Rina, Onodera, Arisa
• Format: Journal Article
• Language: English
• Published: Greece International Institute of Anticancer Research 01.12.2021
• Subjects: Animals; Anisomycin; Anisomycin - pharmacology; Anisomycin - therapeutic use; Anticancer properties; Antitumor activity; Antitumor agents; Cancer; Cell Proliferation; Cytotoxicity; Disease Models, Animal; Gene expression; Genes; Glucose; Glucose metabolism; Humans; In Vitro Techniques; Low concentrations; Melanoma; Melanoma, Experimental - drug therapy; Metabolism; Mice; Molecular modelling; p53 Protein; Protein Synthesis Inhibitors - pharmacology; Protein Synthesis Inhibitors - therapeutic use; Senescence; Spheroids; Toxicity; NAD; TXNIP; glucose; Anisomycin; B16 melanoma cells; spheroid culture
• ISSN: 0250-7005; 1791-7530
• DOI: 10.21873/anticanres.15431

Anisomycin, a potential anticancer therapeutic drug, exerts an antitumor effect on melanoma cells at a lower concentration than that required for other cancer cells. However, the molecular mechanisms remain unclear. The sensitivity to and cytotoxicity of anisomycin, as well as the effects of anisomycin on glucose metabolism and relative mRNA expression of senescence- and cancer-associated genes, were studied using B16 mouse melanoma cells. The viability of anisomycin-treated cells decreased in a concentration-dependent manner, and the growth of cell spheroids was suppressed by 50 nM anisomycin. Glucose metabolism was reduced by anisomycin treatment, and the mRNA expression of genes responsible for growth inhibition, such as p21, p53 and Txnip was upregulated. The results suggest that anisomycin may be a promising future anticancer drug that is effective at low concentrations against melanoma by reducing glucose metabolism, causing cell senescence-like phenomena.