ArticleMolecular biology reports2023
Long non-coding RNA SNHG17 contributes to the progression of pancreatic adenocarcinoma by modulating miR-32-5p/EZH2/STAT3 signaling.
Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed, 3 citations in OpenAlex.
- LncRNA FEZF1-AS1 facilitates cisplatin resistance in non-small cell lung cancer through modulating the miR-32-5p-glutaminase axis.American journal of cancer research · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
backgroundAdenocarcinoma of the pancreas (PAAD) is one of the most malignant tumors in the gastrointestinal tract. Long-chain noncoding RNAs (lncRNAs) are non-coding RNAs that are expressed in a variety of cancers. The purpose of this study is to study the expression, biology functions, and molecular mechanism of lncRNA SNHG17 in PAAD.
methodsIn this study, qRT-PCR was used to measure the relative expression of SNHG17 and miR-32-5p in PAAD. In order to investigate the effect of SNHG17 and miR-32-5p on the proliferation, migration and invasion of PAAD cells, we performed a variety of tests including CCK-8, colony formation, scratch and transwell assays. Furthermore, SNHG17 and miR-32-5p interactions were confirmed by a luciferase reporter gene test.
resultsOur results indicate that the expression of SNHG17 in PAAD is elevated, and in vitro studies have shown that SNHG17 enhances the proliferation of PAAD cells, Mechanistically, it has been shown that SNHG17 can direct target miR-32-5p in PAAD cells, thus promoting the proliferation of PAAD cells, migration, and invasion. Furthermore, SNHG17 has been found to activate EZH2/STAT3 signaling pathway through miR-32-5p in PAAD cells.
conclusionOur results show that SNHG17 plays a key role in the progression of PAAD by activating STAT3 signaling via regulation of miR-32-5p and EZH2.Identifying these new regulatory pathways may shed light on the underlying mechanism of PAAD and offer a potential therapeutic target for this fatal disease.
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