ORIGINAL RESEARCH article
Front. Genet.
Sec. RNA
Volume 16 - 2025 | doi: 10.3389/fgene.2025.1594354
This article is part of the Research TopicHot Topics in Cell Death: Circular and Non-Coding Endogenous RNA in Cancer ProgressionView all 5 articles
Circ-malat1 promotes Gastric cell growth via miR-154-5p/CCND2
Provisionally accepted
- 1Department of Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China
- 2Department of Digestive, Second Affiliated Hospital of Xi’an Medical University, Xi'an, China
- 3Department of Oncology, Shaanxi Provincial Tumor Hospital, Xi'an, China
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Recent studies have shown that circular RNA (circRNA) plays an important role in the development of gastric cancer. However, despite the widespread use of high-throughput sequencing technologies, the function of many circRNAs in gastric cancer remains unclear. In this study, we selected a circ_0002082 (circ-malat1) that is differentially expressed between normal gastric epithelial cells and gastric cancer cells to further investigate its role and molecular mechanisms in regulating gastric cancer development.The study primarily explores the function and molecular mechanisms of circ-malat1 at the cellular and molecular levels. Functional studies reveal that overexpression of circ-malat1 promotes gastric cancer cell growth. Conversely, silencing the expression of circ-malat1 has the opposite effect. Mechanistic studies indicate that circ-malat1 is predominantly expressed in the cytoplasm of gastric cancer cells and can act as a competing endogenous RNA by sequestering miR-154-5p, thereby enhancing CCND2 gene expression. In conclusion, circ-malat1 promotes the development of gastric cancer by competitively binding to miR-154-5p. Based on literature reports, it is speculated that circ-malat1 may also participate in regulation through other pathways, which require further investigation.
Keywords: Keyword Circ-malat1, gastric cancer, cell growth, miR-154-5p, CCND2
Received: 15 Mar 2025; Accepted: 26 Jun 2025.
Copyright: © 2025 Li, Yang, Wang and Nan. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Lina Li, Department of Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China
Kejun Nan, Department of Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China
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