ArticleOncotarget2017
Hsa-miR-429 promotes bladder cancer cell proliferation via inhibiting CDKN2B.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Liquid Biopsy Based Bladder Cancer Diagnostic by Machine Learning.Diagnostics (Basel, Switzerland) · 2025Article
- The role of miR-200 family in the regulation of hallmarks of cancer.Frontiers in oncology · 2022Review
- hsa‑miR‑429 targets CBX8 to promote cell apoptosis in diffuse large B‑cell lymphoma.Molecular medicine reports · 2021Article
- HIG1 domain family member 1A disrupts proliferation, migration, and invasion of colon adenocarcinoma cells.Bioengineered · 2021Article
- Comprehensive Analysis of Correlations in the Expression of miRNA Genes and Immune Checkpoint Genes in Bladder Cancer Cells.International journal of molecular sciences · 2021Article
- Construction of competing endogenous RNA interaction network as prognostic markers in metastatic melanoma.PeerJ · 2021Article
- LncRNA HOXA11-AS drives cisplatin resistance of human LUAD cells via modulating miR-454-3p/Stat3.Cancer science · 2018Article
- MicroRNAs in Smoking-Related Carcinogenesis: Biomarkers, Functions, and Therapy.Journal of clinical medicine · 2018Review
- An integrated analysis of key microRNAs, regulatory pathways and clinical relevance in bladder cancer.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesHsa-miR-429 is increased in bladder cancer. Its roles in bladder cancer are poorly understood.
methodsThe expression levels of hsa-miR-429 and cyclin-dependent kinase inhibitor 2B (CDKN2B) were determined using Real-Time qPCR in a total of 50 patients with bladder cancer. Bladder cancer T24 and 5637 cells were transfected CDKN2B siRNA or hsa-miR-429 mimic. CDKN2B expression levels after transfection were detected by Real-Time qPCR and Western blot assay respectively. Binding sites between hsa-miR-429 and 3'-untranslated region of CDKN2B were confirmed by Dual luciferase reporter assay. Cell proliferation was evaluated using MTT and EdU assays. Cell apoptosis was determined using ELISA assay.
resultsHigher hsa-miR-429 expression levels were associated with higher tumor grade and stage. All patients with low hsa-miR-429 expression survived 5 years, while with high hsa-miR-429 expression, only 58% survived. Hsa-miR-429 and CDKN2B were inversely expressed in bladder cancer. Hsa-miR-429 mimic decreased the expression of CDKN2B at both mRNA and protein levels. The binding site was confirmed between hsa-miR-429 and 3'-untranslated region of CDKN2B. Up-regulation of hsa-miR-429 or down-regulation of CDKN2B promoted cell growth and decreased apoptosis.
conclusionsOur data suggest a mechanism for hsa-miR-429 to play oncogenic roles via inhibiting CDKN2B.
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