ArticleBMC cancer2017
IGF1R activation and the in vitro antiproliferative efficacy of IGF1R inhibitor are inversely correlated with IGFBP5 expression in bladder cancer.
Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Single-cell RNA sequencing identifies potential critical prognostic biomarkers in bladder carcinoma.Scientific reports · 2025Article
- Deletion of endothelial IGFBP5 protects against ischaemic hindlimb injury by promoting angiogenesis.Clinical and translational medicine · 2024Article
- Article
- The role of pregnancy associated plasma protein-A in triple negative breast cancer: a promising target for achieving clinical benefits.Journal of biomedical science · 2024Review
- Transcriptional profile of human thymus reveals IGFBP5 is correlated with age-related thymic involution.Frontiers in immunology · 2024Article
- The Association between Diabetes Medication Use and Tumour Characteristics at Diagnosis in Patients with Urothelial Carcinoma: A Retrospective Registry-Based Study.Bladder cancer (Amsterdam, Netherlands) · 2023Article
- Circular RNA circ_0002137 regulated the progression of osteosarcoma through regulating miR-433-3p/ IGF1R axis.Journal of cellular and molecular medicine · 2022Article
- IGFBP5 is Upregulated and Associated with Poor Prognosis in Colorectal Cancer.International journal of general medicine · 2022Article
- Biological effects and regulation of IGFBP5 in breast cancer.Frontiers in endocrinology · 2022Review
- Liver Expression ofAnimals : an open access journal from MDPI · 2020Article
- The Multi-Faced Role of PAPP-A in Post-Partum Breast Cancer: IGF-Signaling is Only the Beginning.Journal of mammary gland biology and neoplasia · 2020Review
- Comprehensive Analysis of a circRNA-miRNA-mRNA Network to Reveal Potential Inflammation-Related Targets for Gastric Adenocarcinoma.Mediators of inflammation · 2020Article
- Insulin-Like Growth Factor Binding Protein-5 in Physiology and Disease.Frontiers in endocrinology · 2020Review
- Copy number variation (CNV) in theArchives animal breeding · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe insulin growth factor (IGF) pathway has been proposed as a potential therapeutic target in bladder cancer. We characterized the expression of components of the IGF pathway - insulin growth factor receptors (INSR, IGF1R, IGF2R), ligands (INS, IGF1, IGF2), and binding proteins (IGFBP1-7, IGF2BP1-3) - in bladder cancer and its correlation with IGF1R activation, and the anti-proliferative efficacy of an IGF1R kinase inhibitor in this setting.
methodsWe analyzed transcriptomic data from two independent bladder cancer datasets, corresponding to 200 tumoral and five normal urothelium samples. We evaluated the activation status of the IGF pathway in bladder tumors, by assessing IGF1R phosphorylation and evaluating its correlation with mRNA levels for IGF pathway components. We finally evaluated the correlation between inhibition of proliferation by a selective inhibitor of the IGF1R kinase (AEW541), reported in 13 bladder cancer derived cell lines by the Cancer Cell Line Encyclopedia Consortium and mRNA levels for IGF pathway components.
resultsIGF1R expression and activation were stronger in non-muscle-invasive than in muscle-invasive bladder tumors. There was a significant inverse correlation between IGF1R phosphorylation and IGFBP5 expression in tumors. Consistent with this finding, the inhibition of bladder cell line viability by IGF1R inhibitor was also inversely correlated with IGFBP5 expression.
conclusionThe IGF pathway is activated and therefore a potential therapeutic target for non muscle-invasive bladder tumors and IGFBP5 could be used as a surrogate marker for predicting tumor sensitivity to anti-IGF therapy.
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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 Socratic graph.