文献类型：期刊文献

英文题名：The Epstein-Barr virus-miRNA-BART6-5p regulates TGF-β/SMAD4 pathway to induce glycolysis and enhance proliferation and metastasis of gastric cancer cells

作者：Zhao, Xuhui[1];Huang, Xiaomin[1];Dang, Chunyan[2];Wang, Xia[1];Qi, Yujiao[3];Li, Hongling[2]

第一作者：赵小红

通信作者：Li, HL[1]

机构：[1]Gansu Univ Tradit Chinese Med, Clin Med Coll 1, Lanzhou 730000, Peoples R China;[2]Gansu Peoples Hosp, Dept Oncol, Lanzhou 730000, Peoples R China;[3]Ningxia Med Univ, Clin Med Coll, Yinchuan 750004, Ningxia, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Peoples Hosp, Dept Oncol, Lanzhou 730000, Peoples R China.

年份：2024

卷号：32

期号：5

起止页码：999

外文期刊名：ONCOLOGY RESEARCH

收录：;Scopus(收录号：2-s2.0-85191928917);WOS:【SCI-EXPANDED(收录号:WOS:001220262800001)】；

基金：This work supported by National Health Commission Key Laboratory of Gastrointestinal Tumour Diagnosis and Treatment 2022 Master/Postdoctoral Fund Project (NHCDP2022005) ; Gansu Provincial Science and Technology Department Joint Scientific Research Fund Project (23JRRA1545) ; Gansu Provincial Hospital Intra-Hospital Research Fund Project (22GSYYD-37) ; International Co-Operation Project of Gansu Provincial Science and Technology Department (No. 20YF8WA09 6) .

语种：英文

外文关键词：EBV; TGF- beta/SMAD4; Glycolysis; Gastric cancer

摘要：Background: EBV-miR-BARTs exhibit signi fi cant relevance in epithelial tumors, particularly in EBVassociated gastric and nasopharyngeal cancers. However, their speci fi c mechanisms in the initiation and progression of gastric cancer remain insuf fi ciently explored. Material and Methods: Initially, EBV-miRNA-BART6-5p and its target gene SMAD4 expression were assessed in EBV-associated gastric cancer tissues and cell lines. Subsequent transfection induced overexpression of EBV-miRNA-BART6-5p in AGS and MKN-45, and downregulation in EBVpositive cells (SUN -719). The subsequent evaluation aimed to observe their impact on gastric cancer cell proliferation, migration, and glycolytic processes, with the TGF- beta/SMAD4 signaling pathway value clari fi ed using a TGF- beta inhibitor. Results: EBV-miRNA-BART6-5p exhibits pronounced upregulation in EBV-associated gastric cancer tissues and EBV-positive cells, while its target gene SMAD4 demonstrates downregulated expression. Upregulation of it can promote the proliferation and migration of gastric cancer cells. Additionally, We found EBV-miRNA-BART6-5p promotes glycolysis of gastric cancer cells. Inhibition of the TGF- beta/SMAD4 signaling pathway resulted in suppressed proliferation and migration of gastric cancer cells, concomitant with a diminished glycolytic capacity. Conclusion: In this study, we found that EBV-miRNA-BART6-5p can target SMAD4, effectively increasing glycolysis in gastric cancer cells by regulating the TGF- beta/SMAD4 signaling pathway, thereby enhancing the proliferation and metastasis of gastric cancer cells. Our fi ndings may offer new insights into the metabolic aspects of gastric cancer.