ArticleMolecular and cellular biochemistry2020
Overexpression of MYBL2 promotes proliferation and migration of non-small-cell lung cancer via upregulating NCAPH.
Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 45 citations in OpenAlex.
- Non-structural maintenance of chromosome condensin I complex subunit H knockdown suppresses malignant progression of esophageal squamous cell carcinoma via the Wnt/β-catenin signaling pathway.Journal of gastrointestinal oncology · 2026Article
- Comprehensive bioinformatics analysis of NCAPH expression and its clinical importance in endometrial cancer.Oncology letters · 2026Article
- Prognostic value of MYBL2 and its potential implications for immunotherapy: a study of bioinformatics and experimental validation.British journal of cancer · 2026Article
- MYBL2 regulates the expression of CENPF in lung adenocarcinoma and promotes tumor development and metastasis through AKT pathway activation.European journal of medical research · 2025Article
- Cell cycle regulator MYBL2 is a distinct vulnerability in acute myeloid leukemia.Cell death discovery · 2025Article
- Unveiling SNX10: a key player in bladder cancer progression.Translational andrology and urology · 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
- 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
- Clinical Significance of MYBL2 Expression in Hepatocellular Carcinoma: Impact on Overall Survival.OncoTargets and therapy · 2025Article
- QIGTD: identifying critical genes in the evolution of lung adenocarcinoma with tensor decomposition.BioData mining · 2024Article
- From modulation of cellular plasticity to potentiation of therapeutic resistance: new and emerging roles of MYB transcription factors in human malignancies.Cancer metastasis reviews · 2024Review
- NCAPH drives breast cancer progression and identifies a gene signature that predicts luminal a tumour recurrence.Clinical and translational medicine · 2024Article
- MYBL2 is a Novel Independent Prognostic Biomarker and Correlated with TMB in pancreatic cancer.Journal of Cancer · 2024Article
- Genome-wide binding analysis unveils critical implication of B-Myb-mediated transactivation in cancers.International journal of biological sciences · 2024Article
- Multi-omics characterization and machine learning of lung adenocarcinoma molecular subtypes to guide precise chemotherapy and immunotherapy.Frontiers in immunology · 2024Article
- A comprehensive review on lncRNA LOXL1-AS1: molecular mechanistic pathways of lncRNA LOXL1-AS1 in tumorigenicity of cancer cells.Frontiers in oncology · 2024Review
- NCAPH Drives Breast Cancer Progression and Identifies a Gene Signature that Predicts Luminal A Tumor Recurrence.Research square · 2023Article
- Identification and verification of microtubule associated genes in lung adenocarcinoma.Scientific reports · 2023Article
- Non-SMC condensin I complex subunit H participates in anti-programmed cell death-1 resistance of clear cell renal cell carcinomas.Cell proliferation · 2023Article
- Lung Cancer Gene Regulatory Network of Transcription Factors Related to the Hallmarks of Cancer.Current issues in molecular biology · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
MYB Proto-Oncogene Like 2 (MYBL2) is a highly conserved member of the Myb family of transcription factors and plays a critical role in regulating cell proliferation and survival. Here we show that overexpression of MYBL2 is frequently observed in lung adenocarcinoma (LUAD) and significantly correlates with advanced stage and poor patient survival. Knockdown of MYBL2 induced apoptosis in lung cancer cells and resulted in significant inhibition of cell proliferation, migration, and invasion. Notably, we identified Non-SMC Condensin I Complex Subunit H (NCAPH) gene as a direct target of MYBL2. NCAPH expression is highly correlated with that of MYBL2 in LUAD cases and is tightly affected by MYBL2 knockdown or overexpression in vitro. Chromatin immunoprecipitation (ChIP) assays also showed that MYBL2 directly binds to the transcription start site (TSS) of NCAPH. Moreover, we provided evidence that NCAPH functions as an oncogene in lung cancer and overexpression of NCAPH could partially rescue cell death and migration blockage induced by MYBL2 knockdown. Together, these results suggest that overexpression of MYBL2 promotes proliferation and migration of lung cancer cells via upregulating NCAPH, establishing their roles as novel prognostic biomarkers as well as potential therapeutic targets for the disease.
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