A novel approach to regulate glucose uptake in an anaplastic thyroid cancer cell line

• Published in: Endocrine Connections Vol. 14; no. 2
• Main Authors: Heydarzadeh, Shabnam, Moshtaghie, Ali Asghar, Daneshpour, Maryam, Hedayati, Mehdi
• Format: Journal Article
• Language: English
• Published: England Bioscientifica Ltd 01.02.2025; Bioscientifica
• Subjects: anaplastic thyroid cancer; apoptosis; curcumin; glucose transporters; glucose uptake; necrosis
• ISSN: 2049-3614; 2049-3614
• DOI: 10.1530/EC-24-0336

Curcumin's function in affecting cancer metabolic reprogramming remains poorly understood. Herein, we aimed to elucidate a novel link between Curcumin and the glucose uptake metabolism and glucose transporters (GLUTs) status in SW1736 cell line derived from anaplastic thyroid cancer. TheMTT test and flow cytometry was employed to test cell viability and cell death. For glucose uptake detection, ''GOD-PAP'' enzymatic colorimetric assay was applied to measure the direct glucose levels inside of the cells. Determination of GLUT1 and GLUT3 mRNA and protein expression in SW1736 cells was performed by qRT-PCR and western blotting. Also, the scratch wound healing assay was conducted for cell migration. The data indicated that Curcumin-induced cell death is independent of apoptosis in this type of thyroid cancer cell line. Furthermore, significantly reduced GLUT1 and GLUT3 expression was observed after treatment with Curcumin, resulting in the inhibition of glucose uptake (p < 0.05). Scratch assay indicated the inhibition of cell migration in SW1736 cells treated by Curcumin (p < 0.05). It can be concluded that GLUTs as metabolic targets can be blocked specifically by Curcumin for thyroid cancer prevention. Curcumin, as a promising anti-cancer agent, inhibits the growth of SW1736 anaplastic thyroid cancer cell line by regulating glucose uptake pathway and cell death. Altogether, these results suggest that the glucose pathway may be an important target for therapeutic intervention to sensitize tumor cells to cell death process by inhibition of glucose transporters.