文献类型：期刊文献

英文题名：Downregulation of LncRNA CCAT1 Enhances Chemosensitivity in Cisplatin-Resistant Gastric Cancer Cells

作者：Wu, Qiong[1];Zhu, Chenglou[1];Zhao, Tiantian[2];Liu, Tianxiang[1,3];Da, Mingxu[1,2,3]

第一作者：Wu, Qiong

通信作者：Da, M[1];Da, M[2];Da, M[3]

机构：[1]Lanzhou Univ, Sch Clin Med 1, Lanzhou, Peoples R China;[2]Gansu Univ Chinese Med, Sch Clin Med 1, Lanzhou, Peoples R China;[3]Gansu Prov Hosp, Dept Surg Oncol, Lanzhou, Peoples R China

第一机构：Lanzhou Univ, Sch Clin Med 1, Lanzhou, Peoples R China

通信机构：[1]corresponding author), Lanzhou Univ, Sch Clin Med 1, Lanzhou, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Sch Clin Med 1, Lanzhou, Peoples R China;[3]corresponding author), Gansu Prov Hosp, Dept Surg Oncol, Lanzhou, Peoples R China.|[10735]甘肃中医药大学;

年份：2025

卷号：86

期号：1

外文期刊名：DRUG DEVELOPMENT RESEARCH

收录：;Scopus(收录号：2-s2.0-85215598723);WOS:【SCI-EXPANDED(收录号:WOS:001399273800001)】；

基金：This work was supported by the Natural Science Foundation of Gansu Province (grant number 21JR7RA600) and the Gansu Province Youth Science and Technology Fund (grant number 23JRRA1317).

语种：英文

外文关键词：CCAT1; cisplatin; drug-resistant; gastric cancer

摘要：Chemotherapy is an effective treatment for gastric cancer. However, many patients develop resistance to chemotherapeutic agents during clinical treatment. LncRNA CCAT1 has recently been shown to influence cellular resistance to specific chemotherapeutic drugs, but its role in gastric cancer remains underexplored. This study aims to investigate the role of LncRNA CCAT1 in cisplatin resistance in gastric cancer cells and its potential underlying mechanisms. Gastric cancer cell lines with acquired resistance were established. The expression of CCAT1 was assessed in both cisplatin-sensitive and cisplatin-resistant AGS cell lines. CCAT1 expression was knocked down in AGS/DDP cells, and the changes in IC50 values were measured using the Cell Counting Kit-8 (CCK-8) assay. Apoptosis in gastric cancer cells was evaluated by flow cytometry. Additionally, Western blotting was employed to measure the expression levels of PI3K/AKT/mTOR signaling pathway proteins and apoptosis-related proteins in both interference and control groups. RT-qPCR results indicated that CCAT1 expression was significantly elevated in cisplatin-resistant gastric cancer cells compared to non-resistant cells. Similarly, CCK-8 assay results demonstrated that knocking down CCAT1 in resistant cells increased their sensitivity to cisplatin treatment. Flow cytometry and Western blot results further confirmed that silencing CCAT1 promoted apoptosis in these cells. Additionally, the expression of PI3K/AKT/mTOR signaling pathway proteins was higher in resistant cells compared to their sensitive counterparts, and silencing CCAT1 in AGS/DDP cells resulted in reduced expression of these proteins. In conclusion, the above studies demonstrated that LncRNA CCAT1 induced cisplatin resistance in gastric cancer cells.