ArticleOncogene2022
MYBL2 promotes proliferation and metastasis of bladder cancer through transactivation of CDCA3.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 46 citations in OpenAlex.
- FBXW7 Inhibited M2 Macrophage Polarization in Endometrial Cancer by Reducing CCL2 Secretion Through Ubiquitination of MYBL2 Subtitle: The Role of FBXW7 on M2 Macrophage Polarization in EC.Biochemical genetics · 2026Article
- 3D chromatin architecture-related genes orchestrate LUAD evolution and therapy resistance: insights from integrative machine learning and spatial single-cell mapping.Functional & integrative genomics · 2026Article
- MYBL2 impedes cisplatin sensitivity through suppressing GSDME-mediated pyroptosis in lung adenocarcinoma.Cell death discovery · 2026Article
- The role of theTranslational cancer research · 2026Article
- Prognostic value of MYBL2 and its potential implications for immunotherapy: a study of bioinformatics and experimental validation.British journal of cancer · 2026Article
- CircFAT1(e2) acts as a sponge for miR-30e-5p and inhibits glioma progression by regulating MYBL2-mediated cell proliferation.Discover oncology · 2025Article
- ACTG1 driven splicing of P4HB gene enhances EMT and bladder cancer progression.NPJ precision oncology · 2025Article
- Exploring PKMYT1 as a potential marker for colorectal cancer progression through bioinformatics analyses and experimental validation.Scientific reports · 2025Article
- Unveiling SNX10: a key player in bladder cancer progression.Translational andrology and urology · 2025Article
- Malevolent alliance of MYBL2Journal for immunotherapy of cancer · 2025Article
- ECM characterization and 3D bioprinted models of NSCLC for investigating stiffness-dependent tumor behavior and drug response.Materials today. Bio · 2025Article
- Hypoxic HPV-Positive Cancer Cells Are Particularly Sensitive to the Pro-Senescent Effects of B-MYB Repression Due to the Lack of Compensatory A-MYB Induction.Journal of medical virology · 2025Article
- Upregulation of OGT-mediated EZH2 O-GlcNAcylation Promotes Human Umbilical Vein Endothelial Cell Proliferation, Invasion, Migration, and Tube Formation in Gestational Diabetes Mellitus.Cell biochemistry and biophysics · 2025Article
- Dysregulation of MYBL2 impairs extravillous trophoblast lineage development and function, contributing to recurrent spontaneous abortion.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A gene signature associated with cellular senescence serves as an important prognostic indicator in hepatocellular carcinoma.Translational cancer research · 2025Article
- MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cells.Scientific reports · 2025Article
- CDCA3-MYC positive feedback loop promotes bladder cancer progression via ENO1-mediated glycolysis.Journal of experimental & clinical cancer research : CR · 2025Article
- Senescence-specific molecular subtypes stratify the hallmarks of the tumor microenvironment and guide precision medicine in bladder cancer.BMC cancer · 2025Article
- A systems biology approach to unveil shared therapeutic targets and pathological pathways across major human cancers.Computational and structural biotechnology journal · 2025Article
- Comparative bioinformatics analysis of the Wnt pathway in breast cancer: Selection of novel biomarker panels associated with ER status.Open life sciences · 2025Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor MYB proto-oncogene like 2 (MYBL2) is critical in regulating gene expression and tumorigenesis. However, the biological function of MYBL2 in bladder cancer (BLCA) remains to be elucidated. Here, we first revealed that MYBL2 was elevated in BLCA tissues and significantly correlated with clinicopathological parameters and cancer-specific survival in BLCA patients. Phenotypic assays showed that MYBL2 deficiency suppressed the proliferation and migration of BLCA cells in vitro and in vivo, whereas MYBL2 overexpression contributed to the opposite phenotype. Mechanistically, MYBL2 could bind to the promoter of its downstream target gene cell division cycle-associated protein 3 (CDCA3) and transactivate it, which in turn promoted the malignant phenotype of BLCA cells. Further investigations revealed that MYBL2 interacted with forkhead box M1 (FOXM1) to co-regulate the transcription of CDCA3. In addition, MYBL2/FOXM1 and CDCA3 might activate Wnt/β-catenin signaling, thereby promoting the malignant phenotype of BLCA cells. In conclusion, the current study identifies MYBL2 as an oncogene in BLCA. MYBL2 can accelerate the proliferation and metastasis of BLCA through the transactivation of CDCA3.
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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.