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Original Research Article | OPEN ACCESS

Tectorigenin functions as a potential drug for melanoma treatment via inhibition of cell growth, migration and aerobic glycolysis

Qiao Yan, Fei Wang

Department of Dermatology, School of Medicine, ZhongDa Hospital, Southeast University, Nanjing, Jiangsu 210009, China;

For correspondence:-  Fei Wang   Email: fwang5481@163.com   Tel:+862583272170

Accepted: 3 October 2023        Published: 30 October 2023

Citation: Yan Q, Wang F. Tectorigenin functions as a potential drug for melanoma treatment via inhibition of cell growth, migration and aerobic glycolysis. Trop J Pharm Res 2023; 22(10):2075-2080 doi: 10.4314/tjpr.v22i10.8

© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the role of tectorigenin (TG) in melanoma cells.
Methods: Viability of A375 and A2058 melanoma cells was determined by cell counting kit (CCK-8) assay. Cell cycle progression was analyzed by 5-ethynyl-2’-deoxyuridine (EdU) staining. Migration and invasion of melanoma cells were determined by Transwell assay. The epithelial-mesenchymal transition (EMT) of melanoma cells was investigated by determining expression of E-Cadherin and Snail. expression of glucose transporter 1 (GLUT1) and lactose dehydrogenase A (LDHA) was assessed via western blotting. Glucose and lactate production was evaluated by corresponding assay kit. The NOX4 and FOXM1 expressions were determined using western blotting.
Results: Tectorigenin inhibited proliferation, migration and invasion of A375 and A2058 melanoma cells. Tectorigenin regulated cell cycle progression by decreasing the number of cells in S-phase and significantly inhibited snail expression and increased expression of E-Cadherin (p < 0.05), thus inhibiting the EMT of A375 and A2058 cells. Tectorigenin inhibited expression of GLUT1 and LDHA, thereby leading to reduction in glucose consumption and lactate production. It also significantly inhibited expressions of NOX4 and FOXM1 (p < 0.05), indicating an inhibitory effect on the activity of NOX4/FOXM1 pathway.
Conclusion: Tectorigenin inhibits aerobic glycolysis, growth and migration in melanoma cells by suppressing the activity of NOX4/FOXM1 pathway, suggesting its potential in melanoma treatment.

Keywords: Thyroid hormone receptor interactor 13, Gastric cancer, Proliferation, Migration, Stemness, Cisplatin resistance

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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