miR-26a suppresses tumor growth and metastasis by targeting FGF9 in gastric cancer.
prospective_cohort · Level II
Where this comes from
- Record sourced from PubMed, PMID 24015269.
- Also identified by DOI 10.1371/journal.pone.0072662 and PMC identifier 3756000.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
The role of miR-26a in cancer cells seemed controversial in previous studies. Until now, the role of miR-26a in gastric cancer remains undefined. In this study, we found that miR-26a was strongly downregulated in gastric cancer (GC) tissues and cell lines, and its expression levels were associated with lymph node metastasis and clinical stage, as well as overall survival and replase-free survival of GC. We also found that ectopic expression of miR-26a inhibited GC cell proliferation and GC metastasis in vitro and in vivo. We further identified a novel mechanism of miR-26a to suppress GC growth and metastasis. FGF9 was proved to be a direct target of miR-26a, using luciferase assay and western blot. FGF9 overexpression in miR-26a-expressing cells could rescue invasion and growth defects of miR-26a. In addition, miR-26a expression inversely correlated with FGF9 protein levels in GC. Taken together, our data suggest that miR-26a functions as a tumor suppressor in GC development and progression, and holds promise as a prognostic biomarker and potential therapeutic target for GC.
Medical subject headings
- Biomarkers, Tumor
- Cell Proliferation
- Fibroblast Growth Factor 9
- Gene Expression Regulation, Neoplastic
- MicroRNAs
- Neoplasm Proteins
- RNA, Neoplasm
- Stomach Neoplasms