Abstract
The aim of this study was to explore the molecular mechanism through which metformin combined with 2-deoxy-d-glucose (2-DG) decreases the viability of BCPAP thyroid papillary carcinoma cells. BCPAP cells were treated with only metformin, only 2-DG, and both metformin and 2-DG. We used the CCK-8 assay to assess cell viability, dichlorofluorescein staining to detect reactive oxygen species (ROS), and western blot analysis to quantify protein expression. We found that metformin and 2-DG alone decreased cell viability in a time- and dose-dependent manner. The IC50 values of metformin and 2-DG were 5.329 mM and 1.154 mM, respectively. Coadministration of metformin and 2-DG significantly inhibited BCPAP cell proliferation and increased cellular ROS levels and AKT phosphorylation at Ser437. These effects were reversed following the treatment of the cells with N-acetyl-L-cysteine (NAC). Our findings suggest that metformin and 2-DG synergistically suppress BCPAP cell proliferation, potentially via inhibition of the PI3K/AKT signaling pathway by increasing cellular ROS levels.
Keywords: Metformin, 2-Deoxy-d-glucose(2-DG), Reactive oxygen species (ROS), PI3K/AKT signaling pathway, IC50 values
Anti-Cancer Agents in Medicinal Chemistry
Title:Metformin and 2-Deoxy-d-glucose synergistically inhibit the viability of thyroid papillary carcinoma with BRAF mutation by ROS-dependent PI3K/AKT signaling pathway
Volume: 23
Author(s): Xiyuan Lin, Jie Xu, Chi Ma, Zhengzhai Wang, Xiaoqing Yang, Xicheng Song*Haitao Zheng*
Affiliation:
- Department of Otorhinolaryngology, Head and Neck Surgery, Yuhuangding Hospital, Yantai, China
- Department of Thyroid Surgery, Yuhuangding Hospital, Yantai, China
Keywords: Metformin, 2-Deoxy-d-glucose(2-DG), Reactive oxygen species (ROS), PI3K/AKT signaling pathway, IC50 values
Abstract: The aim of this study was to explore the molecular mechanism through which metformin combined with 2-deoxy-d-glucose (2-DG) decreases the viability of BCPAP thyroid papillary carcinoma cells. BCPAP cells were treated with only metformin, only 2-DG, and both metformin and 2-DG. We used the CCK-8 assay to assess cell viability, dichlorofluorescein staining to detect reactive oxygen species (ROS), and western blot analysis to quantify protein expression. We found that metformin and 2-DG alone decreased cell viability in a time- and dose-dependent manner. The IC50 values of metformin and 2-DG were 5.329 mM and 1.154 mM, respectively. Coadministration of metformin and 2-DG significantly inhibited BCPAP cell proliferation and increased cellular ROS levels and AKT phosphorylation at Ser437. These effects were reversed following the treatment of the cells with N-acetyl-L-cysteine (NAC). Our findings suggest that metformin and 2-DG synergistically suppress BCPAP cell proliferation, potentially via inhibition of the PI3K/AKT signaling pathway by increasing cellular ROS levels.
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Lin Xiyuan, Xu Jie, Ma Chi, Wang Zhengzhai, Yang Xiaoqing, Song Xicheng*, Zheng Haitao*, Metformin and 2-Deoxy-d-glucose synergistically inhibit the viability of thyroid papillary carcinoma with BRAF mutation by ROS-dependent PI3K/AKT signaling pathway, Anti-Cancer Agents in Medicinal Chemistry 2023; 23 () . https://dx.doi.org/10.2174/1871520623666230223124733
DOI https://dx.doi.org/10.2174/1871520623666230223124733 |
Print ISSN 1871-5206 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5992 |
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