Heydarzadeh Shabnam, Moshtaghie Ali Asghar, Daneshpour Maryam, Hedayati Mehdi
S Heydarzadeh, Cellular and Molecular Endocrine Research Center, Shahid Beheshti University of Medical Sciences Research Institute for Endocrine Sciences, Tehran, Iran (the Islamic Republic of).
A Moshtaghie, Department of Biochemistry, Islamic Azad University, tehran, Iran (the Islamic Republic of).
Endocr Connect. 2024 Nov 1;14(2). 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.
姜黄素在影响癌症代谢重编程方面的作用仍知之甚少。在此，我们旨在阐明姜黄素与间变性甲状腺癌来源的SW1736细胞系中葡萄糖摄取代谢及葡萄糖转运蛋白（GLUTs）状态之间的新联系。
采用MTT试验和流式细胞术检测细胞活力和细胞死亡情况。对于葡萄糖摄取检测，应用“GOD-PAP”酶比色法测量细胞内的直接葡萄糖水平。通过qRT-PCR和蛋白质印迹法测定SW1736细胞中GLUT1和GLUT3的mRNA及蛋白质表达。此外，进行划痕伤口愈合试验以检测细胞迁移情况。
数据表明，在这种类型的甲状腺癌细胞系中，姜黄素诱导的细胞死亡与凋亡无关。此外，用姜黄素处理后观察到GLUT1和GLUT3表达显著降低，导致葡萄糖摄取受到抑制（p < 0.05）。划痕试验表明，姜黄素处理的SW1736细胞的迁移受到抑制（p < 0.05）。
可以得出结论，作为代谢靶点的GLUTs可被姜黄素特异性阻断以预防甲状腺癌。姜黄素作为一种有前景的抗癌剂，通过调节葡萄糖摄取途径和细胞死亡来抑制间变性甲状腺癌SW1736细胞系的生长。总之，这些结果表明葡萄糖途径可能是通过抑制葡萄糖转运蛋白使肿瘤细胞对细胞死亡过程敏感的治疗干预的重要靶点。
