文献类型：期刊文献

英文题名：Inhibition of Phosphoglycerate Kinase 1 Enhances Radiosensitivity of Esophageal Squamous Cell Carcinoma to X-rays and Carbon Ion Irradiation

作者：Chen, Junru[1,2];Luo, Hongtao[1];Wu, Xun[1,2];Dong, Meng[1,2];Wang, Dandan[1,2];Ou, Yuhong[1,2];Wang, Yuhang[1,2];Sun, Shilong[1];Liu, Zhiqiang[1];Yang, Zhen[3];Guan, Quanlin[2];Zhang, Qiuning[1]

第一作者：Chen, Junru

通信作者：Zhang, QN[1]

机构：[1]Chinese Acad Sci, Inst Modern Phys, Lanzhou 730000, Gansu, Peoples R China;[2]Lanzhou Univ, Sch Clin Med 1, Lanzhou 730000, Gansu, Peoples R China;[3]Gansu Univ Chinese Med, Sch Publ Hlth, Lanzhou 730030, Gansu, Peoples R China

第一机构：Chinese Acad Sci, Inst Modern Phys, Lanzhou 730000, Gansu, Peoples R China

通信机构：[1]corresponding author), Chinese Acad Sci, Inst Modern Phys, Lanzhou 730000, Gansu, Peoples R China.

年份：2025

卷号：30

期号：5

起止页码：36430

外文期刊名：FRONTIERS IN BIOSCIENCE-LANDMARK

收录：;Scopus(收录号：2-s2.0-105008257041);WOS:【SCI-EXPANDED(收录号:WOS:001502157500004)】；

基金：All authors sincerely thank Professor Wang Xiaohu for his guidance in this study.

语种：英文

外文关键词：ionizing radiation; phosphoglycerate kinase 1; reactive oxygen species; radiosensitivity; carbon ions

摘要：Background: Radiotherapy is crucial for managing esophageal squamous cell carcinoma (ESCC). This research explored the potential and mechanism of enhancing ESCC radiosensitivity through targeting phosphoglycerate kinase 1 (PGK1).Methods: After ESCC cells were exposed to X-rays and C-ions, hub genes were identified through proteomic analysis and bioinformatics. To elucidate PGK1's function, small interfering RNAs and plasmids were used to silence and overexpress PGK1 in two human ESCC cell lines. Plate colony formation, cell counting kit 8, and 5-ethynyl-2 '-deoxyuridine assays were conducted to detect cell proliferation after irradiation with different linear energy transfer rays (X-rays and carbon ions). Flow cytometry was used to assess radiation-induced perturbations in the cell cycle, apoptosis, reactive oxygen species (ROS), and mitochondrial membrane potential. Western blotting was performed to detect the protein expressions of protein kinase B (Akt), phosphorylated protein Kinase B (pAkt), mammalian target of rapamycin (mTOR), and phosphorylated mammalian target of rapamycin (pmTOR).Results: Proteomics and bioinformatics analyses revealed that PGK1 plays a key role in modulating ESCC radiosensitivity. Knockdown of PGK1 resulted in the suppression of cancer cell proliferation and viability, promoted apoptotic processes, and demonstrated a synergistic anti-tumor effect in conjunction with radiation. Conversely, overexpression of PGK1 promoted cancer cell growth and increased radiation resistance. This may be attributed to the accumulation of ROS and the inhibition of Akt/mTOR pathway following PGK1 inhibition.Conclusion: Targeting PGK1 may be an effective strategy to increase ESCC radiation sensitivity, offering a promising strategy for improving treatment outcomes.