ArticleThe Journal of biological chemistry2008
Breast cancer metastasis suppressor-1 differentially modulates growth factor signaling.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Pooled it
- A sponge homolog of BRMS1 reveals ancient origin of metastasis-suppressing functions.BMC biology · 2026Article
- Distinct expression and function of breast cancer metastasis suppressor 1 in mutant P53 glioblastoma.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- BRMS1: a multifunctional signaling molecule in metastasis.Cancer metastasis reviews · 2020Review
- Gene expression profiling and DNA methylation analyses of CTCs.Molecular oncology · 2016Review
- Cyclin-dependent kinase-mediated phosphorylation of breast cancer metastasis suppressor 1 (BRMS1) affects cell migration.Cell cycle (Georgetown, Tex.) · 2016Article
- Article
- Microenvironmental Influences on Metastasis Suppressor Expression and Function during a Metastatic Cell's Journey.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2014Article
- Expression of metastasis suppressor BRMS1 in breast cancer cells results in a marked delay in cellular adhesion to matrix.Molecular carcinogenesis · 2014Article
- Imaging of epidermal growth factor receptor on single breast cancer cells using surface-enhanced Raman spectroscopy.Analytica chimica acta · 2014Article
- The roles of the epithelial-mesenchymal transition marker PRRX1 and miR-146b-5p in papillary thyroid carcinoma progression.The American journal of pathology · 2014Article
- Article
- Effect and mechanism of the metastasis suppressor gene BRMS1 on the migration of breast cancer cells.International journal of clinical and experimental medicine · 2013Article
- Low BRMS1 expression promotes nasopharyngeal carcinoma metastasis in vitro and in vivo and is associated with poor patient survival.BMC cancer · 2012Article
- Review
- Ubiquitous Brms1 expression is critical for mammary carcinoma metastasis suppression via promotion of apoptosis.Clinical & experimental metastasis · 2012Article
- Cytoplasmic BRMS1 expression in malignant melanoma is associated with increased disease-free survival.BMC cancer · 2012Article
- Review
- Prognostic significance of BRMS1 expression in human melanoma and its role in tumor angiogenesis.Oncogene · 2011Article
- Patient outcome prediction using multiple biomarkers in human melanoma: A clinicopathological study of 118 cases.Experimental and therapeutic medicine · 2011Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
That metastatic tumor cells grow in selective non-native environments suggests an ability to differentially respond to local microenvironments. BRMS1, like other metastasis suppressors, halts ectopic growth (metastasis) without blocking orthotopic tumor formation. BRMS1-expressing tumor cells reach secondary sites but do not colonize distant tissues, compelling the hypothesis that BRMS1 selectively restricts the ability of tumor cells to respond to exogenous regulators in different tissues. Here we report that BRMS1 expression in metastatic human breast cancer cells leads to a selective reduction in epidermal growth factor receptor expression and downstream (AKT) signaling. Signaling through another receptor tyrosine kinase, hepatocyte growth factor receptor (c-Met), remains unaltered despite reduced levels of the signaling intermediate phosphatidylinositol (4,5)-bisphosphate. Interestingly, reduced downstream calcium signaling is observed following treatment with platelet-derived growth factor, consistent with decreased phosphatidylinositol (4,5)-bisphosphate. However, platelet-derived growth factor receptor expression is unaltered. Thus, BRMS1 differentially attenuates cellular responses to mitogenic signals, not only dependent upon the specific signal received, but at varying steps within the same signaling cascade. Specific modulation of signaling responses received from the microenvironment may ultimately dictate which environments are permissive/restrictive for tumor cell growth and provide insights into the biology underlying metastasis.
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.