ArticleJournal of oncology2021
LncRNA SNHG3 Promotes Gastric Cancer Cells Proliferation, Migration, and Invasion by Targeting miR-326.
Article in Journal of oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- The role of the ceRNA network mediated by lncRNA SNHG3 in the progression of cancer.Discover oncology · 2024Review
- The Functions and Mechanisms of Long Non-coding RNA SNHGs in Gastric Cancer.Combinatorial chemistry & high throughput screening · 2024Review
- Noval ceRNA axis-mediated high expression ofTranslational cancer research · 2023Article
- SNHG3/WISP2 Axis Promotes Hela Cell Migration and InvasionCancer genomics & proteomics · 2023Article
- LINC00960 regulates cell proliferation and glycolysis in pancreatic cancer through the miR-326-3p/TUFT1/AKT-mTOR axis.The Kaohsiung journal of medical sciences · 2022Article
- Small nucleolar RNA host gene 3 functions as a novel biomarker in liver cancer and other tumour progression.World journal of gastroenterology · 2022Review
- Epithelial-mesenchymal transition-related long noncoding RNAs in gastric carcinoma.Frontiers in molecular biosciences · 2022Review
- Corrigendum to "LncRNA SNHG3 Promotes Gastric Cancer Cells Proliferation, Migration, and Invasion by Targeting miR-326".Journal of oncology · 2022Article
- Long noncoding RNA SNHG3 promotes malignant phenotypes in cervical cancer cells via association with YAP1.Human cell · 2022Article
- A comprehensive analysis of ncRNA-mediated interactions reveals potential prognostic biomarkers in prostate adenocarcinoma.Computational and structural biotechnology journal · 2022Article
- METTL3-mediated mInternational journal of immunopathology and pharmacologyArticle
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The function and possible mechanism of lncRNA Small Nucleolar RNA Host Gene 3 (SNHG3) in GC have not been fully studied. The aim of our study was to investigate the role of SNHG3 in the proliferation, migration, and invasion of GC cell lines. The expressions of SNHG3, miR-326, and TWIST in GC9811-P GC cell lines were detected by RT-qPCR. Western blotting was performed to detect the protein levels of TWIST and EMT-related genes. Luciferase reporter gene analysis and RNA immunoprecipitation (RIP) analysis confirmed the interaction between lncRNA SNHG3, miR-326, and TWIST. CCK-8 and Transwell assays were performed to detect cell proliferation, invasion, and migration abilities. The results showed that lncRNA SNHG3 and TWIST were highly expressed in GC cell lines, while miR-326 was expressed to a low degree. Moreover, lncRNA SNHG3 knockdown or miR-326 overexpression significantly inhibited cell proliferation, migration, and invasion of GC cell lines. In addition, TWIST overexpression can reverse the inhibition of lncRNA SNHG3 knockdown or miR-326 overexpression on cell proliferation, migration, and invasion. In conclusion, lncRNA SNHG3 may promote GC progression through the miR-326/TWIST axis, which may provide a new diagnostic and prognostic biomarker for GC.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.