RNA-binding protein ENO1 promotes the tumor progression of gastric cancer by binding to and regulating gastric cancer-related genes

Journal of Gastrointestinal Oncology

article

Na Wang¹  Hui Qiao³  Jianpeng Hao⁴  Chenghui Deng⁴  Nan Zhou¹  Lei Yang⁵  Miaomiao Zeng¹  Quanlin Guan⁴ 

[1]The First Clinical Medical College of Lanzhou University

[2]Department of Oncology, Lanzhou University Second Hospital

[3]Department of Oncology, Lanzhou University First Hospital

[4]Department of Oncology Surgery, Lanzhou University First Hospital

[5]Department of General Surgery, Lanzhou University First Hospital

关键词: RNA-binding protein;    glycolytic pathway enolase 1;    gastric cancer (GC);    pyruvate kinase M2 (PKM2);    glycolysis;   

DOI  :  10.21037/jgo-23-151

学科分类：肿瘤学

来源: Pioneer Bioscience Publishing Company

【 摘 要 】

Background: This study sought to identify the downstream target genes of enolase 1 (ENO1), clarify the role of ENO1 in gastric cancer (GC), and provide novel insights into the regulatory mechanisms of ENO1 in the occurrence and development of GC. Methods: We performed RNA-immunoprecipitation sequencing in MKN-45 cells to study the types and abundance of pre-messenger RNA (mRNA)/mRNA bound by ENO1, the binding sites and motifs, the relationship between ENO1 binding and its regulation of transcription level, and alternative splicing level by combining with RNA-sequencing (RNA-seq) data to further clarify the role of ENO1 in GC. Results: We found that ENO1 stabilized the expression of SRY-box transcription factor 9 (SOX9), vascular endothelial growth factor A (VEGFA), G protein-coupled receptor class C group 5 member A (GPRC5A), and myeloid cell leukemia-1 (MCL1) by binding to their mRNA, which increased the growth of GC. In addition, ENO1 interacted with some other long non-coding RNAs (lncRNAs) or small-molecule kinases, such as NEAT1, LINC00511, CD44, and pyruvate kinase M2 (PKM2), to regulate their expression to affect cell proliferation, migration, and apoptosis. Conclusions: ENO1 may play a role in GC by binding to and regulating GC-related genes. Our findings extend understandings of its mechanism as a clinical therapeutic target.

【 授权许可】

Unknown