ArticlePloS one2013
BMI1 polycomb group protein acts as a master switch for growth and death of tumor cells: regulates TCF4-transcriptional factor-induced BCL2 signaling.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02404480 (A Phase 1 Study of PTC596 in Patients With Advanced Solid Tumors), which is not on this map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Phase 1 Study of PTC596 in Patients With Advanced Solid Tumors
Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
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- Molecular Insight into Prostate Cancer: Preventive Role of Selective Bioactive Molecules.Life (Basel, Switzerland) · 2023Review
- Epigenetic Regulation of Breast Cancer Stem Cells Contributing to Carcinogenesis and Therapeutic Implications.International journal of molecular sciences · 2021Review
- Regulation of gene transcription of B lymphoma Mo-MLV insertion region 1 homolog (Review).Biomedical reports · 2021Review
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- Dehydroxyhispolon Methyl Ether, A Hispolon Derivative, Inhibits WNT/β-Catenin Signaling to Elicit Human Colorectal Carcinoma Cell Apoptosis.International journal of molecular sciences · 2020Article
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- Cellular and Molecular Mechanisms Underlying Prostate Cancer Development: Therapeutic Implications.Medicines (Basel, Switzerland) · 2019Review
- TCF4 induces enzalutamide resistance via neuroendocrine differentiation in prostate cancer.PloS one · 2019Article
- Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Etoposide-resistance in a neuroblastoma model cell line is associated with 13q14.3 mono-allelic deletion and miRNA-15a/16-1 down-regulation.Scientific reports · 2018Article
- A new transgenic mouse model for conditional overexpression of the Polycomb Group protein EZH2.Transgenic research · 2017Article
- Bmi1 inhibition enhances the sensitivity of pancreatic cancer cells to gemcitabine.Oncotarget · 2016Article
- Fusion with stem cell makes the hepatocellular carcinoma cells similar to liver tumor-initiating cells.BMC cancer · 2016Article
- BMI1 is expressed in canine osteosarcoma and contributes to cell growth and chemotherapy resistance.PloS one · 2015Article
- ROBO1, a tumor suppressor and critical molecular barrier for localized tumor cells to acquire invasive phenotype: study in African-American and Caucasian prostate cancer models.International journal of cancer · 2014Article
- Targeting self-renewal, an Achilles' heel of cancer stem cells.Nature medicine · 2014Article
- The S100A4 Oncoprotein Promotes Prostate Tumorigenesis in a Transgenic Mouse Model: Regulating NFκB through the RAGE Receptor.Genes & cancer · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
For advanced prostate cancer (CaP), the progression of tumors to the state of chemoresistance and paucity of knowledge about the mechanism of chemoresistance are major stumbling blocks in the management of this disease. Here, we provide compelling evidence that BMI1 polycomb group protein and a stem cell factor plays a crucial role in determining the fate of tumors vis-à-vis chemotherapy. We show that progressive increase in the levels of BMI1 occurs during the progression of CaP disease in humans. We show that BMI1-rich tumor cells are non-responsive to chemotherapy whereas BMI1-silenced tumor cells are responsive to therapy. By employing microarray, ChIP, immunoblot and Luciferase reporter assays, we identified a unique mechanism through which BMI1 rescues tumor cells from chemotherapy. We found that BMI1 regulates (i) activity of TCF4 transcriptional factor and (ii) binding of TCF4 to the promoter region of anti-apoptotic BCL2 gene. Notably, an increased TCF4 occupancy on BCL2 gene was observed in prostatic tissues exhibiting high BMI1 levels. Using tumor cells other than CaP, we also showed that regulation of TCF4-mediated BCL2 by BMI1 is universal. It is noteworthy that forced expression of BMI1 was observed to drive normal cells to hyperproliferative mode. We show that targeting BMI1 improves the outcome of docetaxel therapy in animal models bearing chemoresistant prostatic tumors. We suggest that BMI1 could be exploited as a potential molecular target for therapeutics to treat chemoresistant tumors.
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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.