ArticleMolecular therapy. Nucleic acids2020
lncRNA SNHG1 Promotes Basal Bladder Cancer Invasion via Interaction with PP2A Catalytic Subunit and Induction of Autophagy.
Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 46 citations in OpenAlex.
- Elevated SNHG1 promotes invasion and migration of Cd(II)-transformed cells through Sox2, Rac1, and Slug.Toxicology and applied pharmacology · 2025Article
- Long non‑coding RNA SNHG1 promotes autophagy in vascular smooth muscle cells induced by facilitating CLEC7A.Molecular medicine reports · 2025Article
- Network Pharmacology Combined with Bioinformatics Analysis to Texplore the Potential Mechanism of Phellodendri Chinensis Cortex Against Bladder Cancer.Cell biochemistry and biophysics · 2024Article
- Tumorigenesis of basal muscle invasive bladder cancer was mediated by PTEN protein degradation resulting from SNHG1 upregulation.Journal of experimental & clinical cancer research : CR · 2024Article
- Autophagy-related lncRNAs in tumor progression and drug resistance: A double-edged sword.Genes & diseases · 2024Review
- Exploration and validation of a novel reactive oxygen species-related signature for predicting the prognosis and chemotherapy response of patients with bladder cancer.Frontiers in immunology · 2024Article
- Long non-coding RNAs: regulators of autophagy and potential biomarkers in therapy resistance and urological cancers.Frontiers in pharmacology · 2024Review
- Circular RNA CCT3 is a unique molecular marker in bladder cancer.BMC cancer · 2023Article
- LncRNA SNHG1: role in tumorigenesis of multiple human cancers.Cancer cell international · 2023Review
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- Long noncoding RNA SNHG1 alleviates high glucose-induced vascular smooth muscle cells calcification/senescence by post-transcriptionally regulating Bhlhe40 and autophagy via Atg10.Journal of physiology and biochemistry · 2023Article
- Long Noncoding RNA HAGLROS Promotes the Malignant Progression of Bladder Cancer by Regulating the miR-330-5p/SPRR1B Axis.Frontiers in oncology · 2022Article
- Tanreqing Injection Attenuates Macrophage Activation and the Inflammatory ResponseFrontiers in immunology · 2022Article
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- SNHG17, as an EMT-related lncRNA, promotes the expression of c-Myc by binding to c-Jun in esophageal squamous cell carcinoma.Cancer science · 2022Article
- Review
- Hypomethylation of PlncRNA-1 promoter enhances bladder cancer progression through the miR-136-5p/Smad3 axis.Cell death & disease · 2020Article
- XIAP's Profile in Human Cancer.Biomolecules · 2020Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Although basal muscle-invasive bladder cancers (MIBCs) are predominant, are more aggressive, and have bad prognoses, molecular mechanisms underlying how basal MIBC formation/progression have been barely explored. In the present study, SNHG1, a long non-coding RNA, was shown to be expressed at higher levels in basal MIBC cells than in other types of bladder BC cells, and its presence could promote basal MIBC cell invasion. The results revealed that SNHG1 specifically induced MMP2 expression via increasing its transcription and mRNA stability. In one mechanism, SNHG1 directly bound with PP2A catalytic subunit (PP2A-c) to inhibit interactions of PP2A-c with c-Jun and then promoted c-Jun phosphorylation that, in turn, mediated MMP2 transcription. In another mechanism, SNHG1 markedly induced autophagy in the cells via induction of increases in the abundance of autophagy-related proteins. The latter initiated autophagy and further abolished miR-34a stability, which reduced overall miR-34a binding directly to the 3' UTR of MMP2 mRNA, thereby promoting MMP2 mRNA stabilization. These results provided novel insight into understanding the specific functions of SNHG1 in basal MIBC. Such findings may ultimately prove highly significant for the design/synthesis of new SNHG1-based compounds for the treatment of basal MIBC patients.
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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 Socratic graph.