Farnesol Inhibits Cell Viability and Activates Apoptosis in Glioma C6 Cells via Downregulating Phosphoinositide 3-kinase (PI3K)/Protein Kinase B (AKT)/Mammalian Target of Rapamycin (mTOR) Pathway

ABSTRACT

Background: Gliomas are the most aggressive and devastating brain tumors, with a poor prognosis due to their complex etiology, diverse clinical manifestations, and the limited efficacy of existing treatment methods. Objectives: The present work was conducted to understand the anticancer activities of farnesol against glioma C6 cells. Materials and Methods: The effects of farnesol on in vitro free radical scavenging were evaluated at various dosages (1–100 μM). A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test was used to assess the influence of farnesol on the growth of glioma C6 cells and nonmalignant Vero cells. The apoptotic levels in the cells were investigated using 4′,6-diamidino-2-phenylindole (DAPI) and dual staining assays. The levels of oxidative stress markers, inflammatory biomarkers, apoptotic protein levels, and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway proteins were assessed using the respective test kits. Results: The results of the free radical scavenging assays proved the antioxidant properties of farnesol. The MTT assay findings demonstrated a significant reduction in C6 cell viability following treatment with farnesol. The findings of the fluorescent assays proved the onset of apoptosis in the farnesol-treated C6 cells. Furthermore, the farnesol treatment effectively increased oxidative stress, increased apoptotic protein levels, and reduced inflammatory marker levels in the C6 glioma cells. The PI3K, AKT, and mTOR protein expression were also successfully downregulated in the C6 glioma cells by farnesol. Conclusion: The current results demonstrate that farnesol effectively suppresses viability and triggers apoptosis in C6 cells. Thus, it has the capacity to be an effective anticancer agent to treat glioma. Nonetheless, additional work is still necessary in the future to determine the specific molecular mechanisms involved in farnesol-induced apoptosis in C6 cells.

KEYWORDS

• Phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway
• oxidative stress
• apoptosis
• farnesol
• glioma

Showing references and in-text citations exactly as published.

• DOI10.1177/09731296241305861Copy

RELATED ARTICLES

Matched on section and article type within this issue of Pharmacogn. Mag..

• Article · VOLUME 21, ISSUE 3Bioflavonoid Tangeretin regulates RANK/RANKL/OPG Signaling Proteins via Stimulating Estrogenic Activity in Ovariectomized RatsWeike Tian, Wei Zhang, Li Chen, Junlei Liao, Xuesong Yang · pp. 1001–1012Original Research ArticleSame type: Article
• Article · VOLUME 21, ISSUE 3PhcogMag 21 3 1013Yanhong Zhang, Yanlong He · pp. 1013–1021Original Research ArticleSame type: Article
• Article · VOLUME 21, ISSUE 3Rosmanol Effectively Prevents Diethylnitrosamine-induced Hepatocellular Carcinoma in Rats by Regulating the PI3K/Akt Signaling PathwayWei Cao, Qi Liu, Ying Wang, Lianfeng Chen · pp. 1022–1033Original Research ArticleSame type: Article
• Article · VOLUME 21, ISSUE 3Liquiritin Promotes Vasodilation Effects by Activating the Kv and KATP Channels in the Isolated Rat Thoracic AortaMengXue Ma, YouLan Che, Xin Yang, Zhi Wang, Ya Wen Bai, Yang Yu, QingBin Xu, Ru Zhou · pp. 1034–1042Original Research ArticleSame type: Article