ArticleTechnology in cancer research & treatment
The Long Non-Coding RNA NEAT1 Promotes Gastric Cancer Cell Proliferation and Invasion by Regulating miR-103a/ STAMBPL1 Axis.
Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 15 citations in OpenAlex.
- Roles of JAMM-family deubiquitinase STAMBPL1 in cellular homeostasis and human cancer.Molecular biology reports · 2026Review
- Unlocking hepatocellular carcinoma aggression: STAMBPL1-mediated TRAF2 deubiquitination activates WNT/PI3K/NF-kb signaling pathway.Biology direct · 2024Article
- Recent advances of NEAT1-miRNA interactions in cancer.Acta biochimica et biophysica Sinica · 2022Review
- NEAT1 as a competing endogenous RNA in tumorigenesis of various cancers: Role, mechanism and therapeutic potential.International journal of biological sciences · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric cancer (GC) is a common malignancy with high morbidity. Long non-coding RNAs (LncRNAs) have been demonstrated to be critical post-transcriptional regulators in tumorigenesis. This study aimed to investigate the effect of LncRNA NEAT1 on the proliferation and metastasis of GC. MATERIAL AND
methodsThe expression of LncRNA NEAT1 was examined in clinical samples and GC cell lines. GC cell lines (SGC-7901 and BGC-823) and human normal gastric epithelial cell line (GES-1) were employed. The correlation between NEAT1, miR-103a and STAMBPL1 was determined by luciferase reporter assay. Cell viability was determined by CCK8 assay. Cell invasion capacity was examined by Transwell assay. The protein level of STAMBPL1 was analyzed by western blotting.
resultsLncRNA NEAT1 was found to be up-regulated in GC cell lines. Further studies identified LncRNA NEAT1 as a direct target of miR-103a. Moreover, NEAT1 knockdown and miR-103a overexpression inhibited cell proliferation and cell invasion. NEAT1 knockdown and miR-103a overexpression also decreased STAMBPL1 levels.
conclusionOur study indicated that LncRNA NEAT1 was up-regulated in GC cells and tissues. NEAT1 was targeted and inhibited by miR-103a and acted as an oncogene, which promoted the malignant behavior of GC cells. This regulatory effect of NEAT1 may be associated with STAMBPL1. Therefore, NEAT1 could be used as a biomarker for predicting the progression of GC.
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Registered trials
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