文献类型：期刊文献

英文题名：Aldo-keto reductase family 1 member C3 mediates radioresistance of esophageal cancer cells through suppressing MAPK and AKT signaling

作者：Xiong, Wei[1,8];Xie, Ya[2];Wang, Dong[2];Huang, Xiaozhi[1];Hao, Xiaohui[3];Liu, Jianming[4];Liu, Xiaohui[4];Gu, Xiaobin[5];Sun, Shaoqian[6];Li, Yufeng[7,8];Li, Jingwu[4,8]

第一作者：Xiong, Wei

通讯作者：Li, JW[1];Li, JW[2]

机构：[1]Tangshan Peoples Hosp, Dept Radiat Oncol, Tangshan 063001, Hebei, Peoples R China;[2]Zhengzhou Univ, Affiliated Hosp 1, Dept Gynecol, Zhengzhou 450052, Henan, Peoples R China;[3]North China Univ Sci & Technol, Sch Publ Hlth, Tangshan 063210, Peoples R China;[4]Tangshan Peoples Hosp, Dept Gastroenterol Surg, Tangshan 063001, Hebei, Peoples R China;[5]Zhengzhou Univ, Affiliated Hosp 1, Dept Radiat Oncol, Zhengzhou, Peoples R China;[6]Beijing Union Univ, Biochem Engn Coll, Beijing 100023, Peoples R China;[7]Tangshan Peoples Hosp, Canc Inst, Tangshan 063001, Hebei, Peoples R China;[8]Tangshan Peoples Hosp, Hebei Key Lab Mol Oncol, Tangshan, Peoples R China

第一机构：Tangshan Peoples Hosp, Dept Radiat Oncol, Tangshan 063001, Hebei, Peoples R China

通讯机构：[1]corresponding author), Tangshan Peoples Hosp, Dept Gastroenterol Surg, Tangshan 063001, Hebei, Peoples R China;[2]corresponding author), Tangshan Peoples Hosp, Hebei Key Lab Mol Oncol, Tangshan, Peoples R China.

年份：2024

卷号：24

期号：1

外文期刊名：BMC CANCER

收录：;Scopus(收录号：2-s2.0-85205786214);WOS:【SCI-EXPANDED(收录号:WOS:001327764200005)】；

基金：This work was supported by the National Natural Science Foundation of China [grant number 81502127], "Study on the mechanism of silencing Akr1C3 gene to reverse radiation resistance of esophageal carcinoma". The funder had no role in the study design, data collection, analysis, interpretation, writing of the report, or decision to submit the paper for publication.

语种：英文

外文关键词：Radiosensitivity; Esophageal cancer; Aldo-keto reductase family 1 member C3; ERK; JNK

摘要：BackgroundAldo-keto reductase family 1 member C3 (AKR1C3) is a radioresistance gene in esophageal cancer. This study aimed to investigate the signaling pathways that mediate the regulatory role of AKR1C3 in the radioresistance of esophageal cancer cells.MethodsThe protein levels of AKR1C3 in cancer tissue samples were compared between patients with radiosensitive and radioresistant esophageal cancer using immunohistochemical staining. AKR1C3-silenced stable KYSE170R esophageal cancer cells (KY170R-shAKR1C3) were established. Colony formation assay was employed to evaluate the radiosensitivity of cancer cells, while flow cytometry analysis was utilized to quantify reactive oxygen species (ROS) production in these cells. Additionally, Western blotting was conducted to determine protein expression levels.ResultsAKR1C3 protein exhibited significantly higher expression in radioresistant cancer tissue samples compared to radiosensitive samples. AKR1C3 silencing promoted radiosensitivity and ROS production of KYSE170R cells. At 32 h after X-ray radiation, the levels of total and phosphorylated ERK1/2, JNK, and AKT proteins were significantly elevated in KYSE170R-shAKR1C3 cells compared to untransfected KYSE170R cells. The inhibitor of AKR1C3 remarkably enhanced the radiosensitivity of KYSE170R cells. Conversely, treatment with either a MEK inhibitor or an AKT inhibitor significantly increased the radioresistance of KYSE170R-shAKR1C3 cells.ConclusionsOur results suggest that AKR1C3 mediates radioresistance of KYSE170R cells possibly through MAPK and AKT signaling.