ArticleOncogene2009
BMI1 cooperates with H-RAS to induce an aggressive breast cancer phenotype with brain metastases.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 100 citations in OpenAlex.
- A palmitate-rich metastatic niche enables metastasis growth via p65 acetylation resulting in pro-metastatic NF-κB signaling.Nature cancer · 2023Article
- Review
- A protein interaction landscape of breast cancer.Science (New York, N.Y.) · 2021Article
- Comparative evaluation of BMI-1 proto-oncogene expression in normal tissue, adenoma and papillary carcinoma of human thyroid in pathology samples.BMC research notes · 2021Article
- Non-Coding RNAs in Normal B-Cell Development and in Mantle Cell Lymphoma: From Molecular Mechanism to Biomarker and Therapeutic Agent Potential.International journal of molecular sciences · 2021Review
- The Role of Polycomb Group Protein BMI1 in DNA Repair and Genomic Stability.International journal of molecular sciences · 2021Review
- Article
- Internal Ribosome Entry Sites Mediate Cap-Independent Translation of Bmi1 in Nasopharyngeal Carcinoma.Frontiers in oncology · 2020Article
- ERK2 regulates epithelial-to-mesenchymal plasticity through DOCK10-dependent Rac1/FoxO1 activation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- A new view of the mammary epithelial hierarchy and its implications for breast cancer initiation and metastasis.Journal of cancer metastasis and treatment · 2019Article
- RAS as Supporting Actor in Breast Cancer.Frontiers in oncology · 2019Review
- Inhibition of BMI1, a Therapeutic Approach in Endometrial Cancer.Molecular cancer therapeutics · 2018Article
- Timosaponin A-III inhibits oncogenic phenotype via regulation of PcG protein BMI1 in breast cancer cells.Molecular carcinogenesis · 2018Article
- Article
- Circ0043898 acts as a tumor inhibitor and performs regulatory effect on the inhibition of esophageal carcinoma.Cancer biology & therapy · 2018Article
- Epigenetic modification of miR-663 controls mitochondria-to-nucleus retrograde signaling and tumor progression.The Journal of biological chemistry · 2017Article
- Proline metabolism supports metastasis formation and could be inhibited to selectively target metastasizing cancer cells.Nature communications · 2017Article
- Risk Factors and Preventions of Breast Cancer.International journal of biological sciences · 2017Review
- Oncogenic Ras: A double-edged sword for human epidermal stem and transient amplifying cells.Small GTPases · 2016Review
- A miR-200c/141-BMI1 autoregulatory loop regulates oncogenic activity of BMI1 in cancer cells.Oncotarget · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
B-lymphoma Moloney murine leukaemia virus insertion region-1 (BMI1) is a member of the polycomb group of transcription repressors, which functions in stem cell maintenance and oncogenesis through the inhibition of the INK4A/ARF tumour suppressor locus. Overexpression of BMI1 is associated with poor prognosis in several human cancers, including breast cancer. We have previously shown that BMI1 collaborates with H-RAS to induce transformation of MCF10A human mammary epithelial cells through dysregulation of multiple growth pathways independent of the INK4A/ARF locus. In this study, we show that BMI1 collaborates with H-RAS to promote increased proliferation, invasion and resistance to apoptosis in vitro, and an increased rate of spontaneous metastases from mammary fat pad xenografts including novel metastases to the brain. Furthermore, in collaboration with H-RAS, BMI1 induced fulminant metastatic disease in the lung using a tail vein model of haematogenous spread through accelerated cellular proliferation and inhibition of apoptosis. Finally, we show that knockdown of BMI1 in several established breast cancer cell lines leads to decreased oncogenic behaviour in vitro and in vivo. In summary, BMI1 collaborates with H-RAS to induce an aggressive and metastatic phenotype with the unusual occurrence of brain metastasis, making it an important target for diagnosis and treatment of aggressive breast cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.