LncRNA CASC2 Inhibits Progression of Glioblastoma by Regulating the Expression of AKT in T98G Cell Line, Treated by TMZ and Thiosemicarbazone Complex

Shahmir, Shohreh; Zahmatkesh, Neda; Mirzaahmadi, Sina; Asaadi Tehrani, Golnaz

doi:10.31557/APJCP.2023.24.5.1553

LncRNA CASC2 Inhibits Progression of Glioblastoma by Regulating the Expression of AKT in T98G Cell Line, Treated by TMZ and Thiosemicarbazone Complex

Document Type : Research Articles

Authors

Department of Genetics, Zanjan Branch, Islamic Azad University, Zanjan, Iran.

10.31557/APJCP.2023.24.5.1553

Abstract

Background: The aim of this study was to evaluate the expression alterations of CACS2 and its target gene, AKT, in T98G cell line treated with Temozolomide and Thiosemicarbazone complex (Ni, Cu) and to compare the results with each other. Methods: Temozolomide and Thiosemicarbazone complexes were prepared in different concentrations. Cell culturing of T98G cell line was carried out and was classified into 3 groups based on the incubation time (24, 48, and 72h) with utilized agents, after RNA extraction the expression level of CACS2 and AKT genes were evaluated by Real-time PCR. Ultimately, the results were analyzed by Rest software. Results: CASC2 expression under Temozolomide treatment at different concentrations (100, 150, 200, and 250 µM) and different time periods (24, 48, and 72h) was increased. Moreover, its expression was significantly upregulated after treating with Ni at the concentrations of 100.5 and 104 µM after 24h. Furthermore, its expression was augmented after 72 h Cu treatment at the concentrations of 15, 16, 17, and 18 µM. In addition, AKT expression after Temozolomide and Thiosemicarbazone complex treatment was significantly decreased (P <0.001). The results showed that the expression alterations of CASC2 and its target gene, AKT, after treatment with Temozolomide and Thiosemicarbazone are highly depended on incubation time and concentration. Conclusion: In a conclusion, the studied agents at different concentrations and times showed a high potential to control the expression of the studied lncRNA and gene in glioblastoma cells.

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