ArticleCancer cell international2017
Pharmacological inhibition of Bmi1 by PTC-209 impaired tumor growth in head neck squamous cell carcinoma.
Article in Cancer cell international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 54 citations in OpenAlex.
- Key Early Changes in Oral Squamous Cell Carcinogenesis Are Accelerated by Ectopic BMI1 Expression.Cancer research communications · 2026Article
- Exogenous BMI1 expression aggravates oral squamous cell carcinomas in tongue epithelia.Neoplasia (New York, N.Y.) · 2025Article
- Review
- The transcription factor BMI1 increases hypoxic signaling in oral cavity epithelia.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- A prognostic model for Schistosoma japonicum infection-associated liver hepatocellular carcinoma: strengthening the connection through initial biological experiments.Infectious agents and cancer · 2024Article
- The Crucial Roles of Bmi-1 in Cancer: Implications in Pathogenesis, Metastasis, Drug Resistance, and Targeted Therapies.International journal of molecular sciences · 2022Review
- Targeting Cancer Stem Cells through Epigenetic Modulation of Interferon Response.Journal of personalized medicine · 2022Review
- Exosomes: Potential Biomarkers and Functions in Head and Neck Squamous Cell Carcinoma.Frontiers in molecular biosciences · 2022Review
- Article
- The Systematic Analyses of RING Finger Gene Signature for Predicting the Prognosis of Patients with Hepatocellular Carcinoma.Journal of oncology · 2022Article
- Inhibition of BMI-1 Induces Apoptosis through Downregulation of DUB3-Mediated Mcl-1 Stabilization.International journal of molecular sciences · 2021Article
- Cancer Stem Cells in Oropharyngeal Cancer.Cancers · 2021Review
- Oral Cancer Stem Cells: Therapeutic Implications and Challenges.Frontiers in oral health · 2021Review
- HPVTranslational oncology · 2021Review
- BMI1 in the heart: Novel functions beyond tumorigenesis.EBioMedicine · 2021Review
- Senescence Induced by BMI1 Inhibition Is a Therapeutic Vulnerability in H3K27M-Mutant DIPG.Cell reports · 2020Article
- A genome-wide enrichment screen identifies NUMA1-loss as a resistance mechanism against mitotic cell-death induced by BMI1 inhibition.PloS one · 2020Article
- Cancer stem cells and oral cancer: insights into molecular mechanisms and therapeutic approaches.Cancer cell international · 2020Review
- Targeting cancer stem cells in squamous cell carcinoma.Precision clinical medicine · 2019Review
- Co-inhibition of BMI1 and Mel18 enhances chemosensitivity of esophageal squamous cell carcinomaOncology letters · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBmi1 (B lymphoma Mo-MLV insertion region 1 homolog) contributes to human tumorigenesis via epigenetic transcriptional silencing and represents a novel therapeutic target with great potentials. Here we sought to determine the therapeutic efficiency of PTC-209, a potent and selective Bmi1 inhibitor, in head neck squamous cell carcinoma (HNSCC) cells and a HNSCC xenograft model.
methodsThe mutation pattern, mRNA level of Bmi1 in HNSCC and its associations with clinicopathological parameters were determined through comprehensive data mining and interrogation using publicly available databases GENT, cBioPortal, Oncomine and TCGA. The PTC-209, a selective and potent Bmi1 inhibitor, was exploited and its effect on Bmi1 expression was measured in two HNSCC cell lines Cal27 and FaDu. The phenotypical changes of HNSCC cells were observed upon PTC-209 treatment in vitro. Moreover, the therapeutic effects of PTC-209 for HNSCC were determined in a xenograft animal model.
resultsThrough comprehensive data mining and interrogation, we found that Bmi1 mRNA was frequently overexpressed in a subset of HNSCC samples. Our data revealed that PTC-209 robustly reduced the expression of Bmi1 in Cal27 and FaDu cells presumably by post-transcriptional repression and ubiquitin-proteasomal degradation. PTC-209 treatment resulted in impaired cell proliferation, G1-phase cell cycle arrest, compromised migration and invasiveness, and increased cell apoptosis and chemosensitivity to 5-FU and cisplatin in vitro. Moreover, PTC-209 exposure reduced colony formation, tumorsphere formation and the percentage of ALDH1
conclusionsOur findings indicate that pharmacological inhibition of Bmi1 is a novel therapeutic strategy for HNSCC patients, especially with those with aberrant Bmi1 overexpression.
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