ArticleBritish journal of cancer2014
Co-targeting the IGF system and HIF-1 inhibits migration and invasion by (triple-negative) breast cancer cells.
Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Targeting RSK2 enhances the efficacy of IGF1R inhibitor against triple-negative breast cancer via antagonizing IGF1/IGF1R signaling mediated by GATA3-IGFBP5 pathway.Acta pharmacologica Sinica · 2026Article
- Coordinated regulation of IGF1R by HIF1α and HIF2α enhances chemoresistance in glioblastoma.Frontiers in pharmacology · 2025Article
- Integration of Gastric Cancer RNA-Seq Datasets Along With PPI Network Suggests That Nonhub Nodes Have the Potential to Become Biomarkers.Cancer reports (Hoboken, N.J.) · 2025Article
- miR-877-5p as a Potential Link between Triple-Negative Breast Cancer Development and Metabolic Syndrome.International journal of molecular sciences · 2023Article
- Multifaceted Interplay between Hormones, Growth Factors and Hypoxia in the Tumor Microenvironment.Cancers · 2022Review
- Transcriptomic profiling of Gh/Igf system reveals a prompted tissue-specific differentiation and novel hypoxia responsive genes in gilthead sea bream.Scientific reports · 2021Article
- Design and preparation of a new multi-targeted drug delivery system using multifunctional nanoparticles for co-delivery of siRNA and paclitaxel.Journal of pharmaceutical analysis · 2021Article
- Sensitization of Carboplatinum- and Taxol-Resistant High-Grade Serous Ovarian Cancer Cells Carrying p53, BRCA1/2 Mutations by Emblica officinalis (Amla) via Multiple Targets.Journal of Cancer · 2020Article
- Carbonic Anhydrase 12 Protects Endplate Cartilage From Degeneration Regulated by IGF-1/PI3K/CREB Signaling Pathway.Frontiers in cell and developmental biology · 2020Article
- Estrogen receptor-beta is a potential target for triple negative breast cancer treatment.Oncotarget · 2018Article
- Sensitization of keloid fibroblasts by quercetin through the PI3K/Akt pathway is dependent on regulation of HIF-1α.American journal of translational research · 2018Article
- Protegrin 1 Enhances Innate Cellular Defense via the Insulin-Like Growth Factor 1 Receptor Pathway.Frontiers in cellular and infection microbiology · 2018Article
- Receptors for Insulin-Like Growth Factor-2 and Androgens as Therapeutic Targets in Triple-Negative Breast Cancer.International journal of molecular sciences · 2017Article
- Revisiting the IGF-1R as a breast cancer target.NPJ precision oncology · 2017Article
- Article
- The insulin-like growth factor-I receptor (IGF-IR) in breast cancer: biology and treatment strategies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- HIF-1 at the crossroads of hypoxia, inflammation, and cancer.International journal of cancer · 2016Review
- Molecular targets of luteolin in cancer.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2016Review
- BMS-536924, an ATP-competitive IGF-1R/IR inhibitor, decreases viability and migration of temozolomide-resistant glioma cells in vitro and suppresses tumor growth in vivo.OncoTargets and therapy · 2015Article
- Insulin-like growth factor system in cancer: novel targeted therapies.BioMed research international · 2015Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMetastatic triple-negative breast cancer is mostly incurable, due to lack of suitable drug targets. The insulin-like growth factor (IGF) system could provide such a target, and IGF-1 receptor (IGF-1R)-directed agents are already available, but seem unable to control all the complexities of the system, including crosstalk with hypoxia-inducible pathways.
methodsMigration of triple-negative MDA-231 breast cancer cells and its modulation by IGFs, the IGF-1R inhibitor NVP-AEW541 and the IGF-2-sequestering monoclonal antibody MAB292 were assessed by the scratch wound healing and Boyden chamber assays; the effect of topotecan (inhibiting hypoxia-inducible factor-1 (HIF-1)) under hypoxia was also evaluated. Constitutive as well as drug-modulated levels of components of the IGF and HIF-1 pathways were evaluated by western blotting and qPCR.
resultsIGF-induced migration of MDA-231 cells was not abrogated by the IGF-1R inhibitor NVP-AEW541, whereas IGF-2 sequestration by MAB292 significantly reduced cell migration. Under hypoxia, topotecan was also effective, likely by reducing HIF-1-induced IGF-2 release. Simultaneous targeting of IGF-1R and IGF-2 or HIF-1 completely abolished cell migration.
conclusionsIR activation may account for the failure of NVP-AEW541 to suppress MDA-231 cell migration. Ligand-targeting compounds, or co-inhibition of the IGF and HIF-1 systems, may prevent activation of compensatory signalling, thereby providing a valuable addition to IGF-1R inhibitor-based therapies.
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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 OpenQuestion graph.