ArticleGenes & development2016
BMI1 induces an invasive signature in melanoma that promotes metastasis and chemoresistance.
Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- The histone demethylase PHF8 regulates TGFβ signaling and promotes melanoma metastasis.Science advances · 2022Pooled it
- BMI1 is required for melanocyte stem cell maintenance and hair pigmentation.Pigment cell & melanoma research · 2023Article
- Epigenetic Mechanisms Underlying Melanoma Resistance to Immune and Targeted Therapies.Cancers · 2022Review
- Ornidazole suppresses CD133+ melanoma stem cells via inhibiting hedgehog signaling pathway and inducing multiple death pathways in a mouse model.Croatian medical journal · 2022Article
- Epigenetic regulator BMI1 promotes alveolar rhabdomyosarcoma proliferation and constitutes a novel therapeutic target.Molecular oncology · 2021Article
- Polycomb complexes redundantly maintain epidermal stem cell identity during development.Genes & development · 2021Article
- Article
- Melanoma Plasticity: Promoter of Metastasis and Resistance to Therapy.Frontiers in oncology · 2021Review
- Comprehensive Exome Analysis of Immunocompetent Metastatic Head and Neck Cancer Models Reveals Patient Relevant Landscapes.Cancers · 2020Article
- Tissue microRNA expression profiling in hepatic and pulmonary metastatic melanoma.Melanoma research · 2020Article
- YAP Enhances Tumor Cell Dissemination by Promoting Intravascular Motility and Reentry into Systemic Circulation.Cancer research · 2020Article
- Article
- Targeting the cyclin-dependent kinase 5 in metastatic melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Predicting the Risk of Melanoma Metastasis Using an Immune Risk Score in the Melanoma Cohort.Frontiers in bioengineering and biotechnology · 2020Article
- Bmi1 Severs as a Potential Tumor-Initiating Cell Marker and Therapeutic Target in Esophageal Squamous Cell Carcinoma.Stem cells international · 2020Article
- Co-delivery of Bmi1 small interfering RNA with ursolic acid by folate receptor-targeted cationic liposomes enhances anti-tumor activity of ursolic acidDrug delivery · 2019Article
- CRISPR-Cas9 Knockdown and Induced Expression of CD133 Reveal Essential Roles in Melanoma Invasion and Metastasis.Cancers · 2019Article
- Phenotype plasticity as enabler of melanoma progression and therapy resistance.Nature reviews. Cancer · 2019Review
- Co-inhibition of BMI1 and Mel18 enhances chemosensitivity of esophageal squamous cell carcinomaOncology letters · 2019Article
- High glucose promotes pancreatic cancer cells to escape from immune surveillance via AMPK-Bmi1-GATA2-MICA/B pathway.Journal of experimental & clinical cancer research : CR · 2019Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Melanoma can switch between proliferative and invasive states, which have identifying gene expression signatures that correlate with good and poor prognosis, respectively. However, the mechanisms controlling these signatures are poorly understood. In this study, we identify BMI1 as a key determinant of melanoma metastasis by which its overexpression enhanced and its deletion impaired dissemination. Remarkably, in this tumor type, BMI1 had no effect on proliferation or primary tumor growth but enhanced every step of the metastatic cascade. Consistent with the broad spectrum of effects, BMI1 activated widespread gene expression changes, which are characteristic of melanoma progression and also chemoresistance. Accordingly, we showed that up-regulation or down-regulation of BMI1 induced resistance or sensitivity to BRAF inhibitor treatment and that induction of noncanonical Wnt by BMI1 is required for this resistance. Finally, we showed that our BMI1-induced gene signature encompasses all of the hallmarks of the previously described melanoma invasive signature. Moreover, our signature is predictive of poor prognosis in human melanoma and is able to identify primary tumors that are likely to become metastatic. These data yield key insights into melanoma biology and establish BMI1 as a compelling drug target whose inhibition would suppress both metastasis and chemoresistance of melanoma.
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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.