ArticleMolecular therapy. Nucleic acids2018
MicroRNA-411 Downregulation Enhances Tumor Growth by Upregulating MLLT11 Expression in Human Bladder Cancer.
Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Causal effect of thyroid cancer on secondary primary malignancies: findings from the UK Biobank and FinnGen cohorts.Frontiers in immunology · 2024Pooled it
- AF1q is a universal marker of neuroblastoma that sustains N-Myc expression and drives tumorigenesis.Oncogene · 2024Article
- MLLT11 Regulates Endometrial Stroma Cell Adhesion, Proliferation and Survival in Ectopic Lesions of Women with Advanced Endometriosis.International journal of molecular sciences · 2023Article
- Enhanced MCM5 Level Predicts Bad Prognosis in Acute Myeloid Leukemia.Molecular biotechnology · 2023Article
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- Novel biomarkers predict prognosis and drug-induced neuroendocrine differentiation in patients with prostate cancer.Frontiers in endocrinology · 2022Article
- Emerging Evidence of the Functional Impact of the miR379/miR656 Cluster (C14MC) in Breast Cancer.Biomedicines · 2021Review
- miR-190 promotes malignant transformation and progression of human urothelial cells through CDKN1B/p27 inhibition.Cancer cell international · 2021Article
- Alkaline phosphatase downregulation promotes lung adenocarcinoma metastasis via the c-Myc/RhoA axis.Cancer cell international · 2021Article
- Oncogenic role ofAutophagy · 2021Article
- Upregulated miR‑411‑5p levels promote lymph node metastasis by targeting RYBP in head and neck squamous cell carcinoma.International journal of molecular medicine · 2021Article
- Coiled-Coil Domain-Containing 68 Downregulation Promotes Colorectal Cancer Cell Growth by Inhibiting ITCH-Mediated CDK4 Degradation.Frontiers in oncology · 2021Article
- uc.77- Downregulation Promotes Colorectal Cancer Cell Proliferation by Inhibiting FBXW8-Mediated CDK4 Protein Degradation.Frontiers in oncology · 2021Article
- MicroRNAs and target molecules in bladder cancer.Medical oncology (Northwood, London, England) · 2020Review
- Pan-cancer analysis of somatic mutations in miRNA genes.EBioMedicine · 2020Article
- Article
- MiR-212-3p inhibits cell proliferation and promotes apoptosis by targeting nuclear factor IA in bladder cancer.Journal of biosciences · 2019Article
- MicroRNA-3648 Is Upregulated to Suppress TCF21, Resulting in Promotion of Invasion and Metastasis of Human Bladder Cancer.Molecular therapy. Nucleic acids · 2019Article
- miR-3687 Overexpression Promotes Bladder Cancer Cell Growth by Inhibiting the Negative Effect of FOXP1 on Cyclin E2 Transcription.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- SNHG8 is upregulated in esophageal squamous cell carcinoma and directly sponges microRNA-411 to increase oncogenicity by upregulating KPNA2.OncoTargets and therapy · 2019Article
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Although several previous studies have reported the implication of various microRNAs (miRNAs) in regulation of human bladder cancer (BC) development, alterations and function of many miRNAs in bladder cancer growth are not explored yet at present. Here, we screened 1,900 known miRNAs and first discovered that miR-411 was one of the major miRNAs, which was down-regulated in n-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN)-induced BCs. This miR-411 down-regulation was also observed in human BC tissues and cell lines. The results from evaluating the relationship between miR-411 and patient survival in BC using the TCGA (The Cancer Genome Atlas) database indicated that miR-411 was positively correlated with DFS (disease-free survival). Our studies also showed that miR-411 inhibited tumor growth of human BC cells in a xenograft animal model. Mechanistic studies revealed that overexpression of miR-411 repressed the expression of ALL1-fused gene from the chromosome 1q (AF1q) (MLLT11) by binding to the 3' untranslated region (UTR) of mllt11 mRNA and in turn induced p21 expression and caused cell cycle arrest at the G2/M phase, further inhibiting BC tumor growth. Collectively, our results improve our understanding of the role of miR-411 in BC tumor growth and suggest miR-411 and MLLT11 as potential new targets for the treatment of BC patients.
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