ReviewFrontiers in endocrinology2015
IGF-1 Receptor and Adhesion Signaling: An Important Axis in Determining Cancer Cell Phenotype and Therapy Resistance.
Review in Frontiers in endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 58 citations in OpenAlex.
- Insulin-like growth factor 1 receptor regulates breast cancer cell adhesion through beta-1 integrin.Frontiers in endocrinology · 2026Article
- Insulin-Like Growth Factor 1 Receptor Regulates Breast Cancer Cell Adhesion through Beta-1 Integrin.bioRxiv : the preprint server for biology · 2025Article
- IGF1R Promotes Th17/Treg Cell Development in Experimental Autoimmune Prostatitis.Journal of inflammation research · 2025Article
- IGF1R signaling induces epithelial-mesenchymal plasticity via ITGAV in cutaneous carcinoma.Journal of experimental & clinical cancer research : CR · 2024Article
- RHOAScience signaling · 2023Article
- IGF-1R targeting in cancer - does sub-cellular localization matter?Journal of experimental & clinical cancer research : CR · 2023Review
- Review
- Integrin signaling is critical for myeloid-mediated support of T-cell acute lymphoblastic leukemia.Nature communications · 2023Article
- Leucine-973 is a crucial residue differentiating insulin and IGF-1 receptor signaling.The Journal of clinical investigation · 2023Article
- Insulin-like growth factors and aging: lessons from Laron syndrome.Frontiers in endocrinology · 2023Review
- Article
- Cannabidiol Antiproliferative Effect in Triple-Negative Breast Cancer MDA-MB-231 Cells Is Modulated by Its Physical State and by IGF-1.International journal of molecular sciences · 2022Article
- Cubilin-, megalin-, and Dab2-dependent transcription revealed by CRISPR/Cas9 knockout in kidney proximal tubule cells.American journal of physiology. Renal physiology · 2022Article
- PDLIM2 is highly expressed in Breast Cancer tumour-associated macrophages and is required for M2 macrophage polarization.Frontiers in oncology · 2022Article
- PDLIM2: Signaling pathways and functions in cancer suppression and host immunity.Biochimica et biophysica acta. Reviews on cancer · 2021Review
- PDLIM2 prevents the malignant phenotype of hepatocellular carcinoma cells by negatively regulating β-catenin.Cancer gene therapy · 2021Article
- Malignant Ascites Promote Adhesion of Ovarian Cancer Cells to Peritoneal Mesothelium and Fibroblasts.International journal of molecular sciences · 2021Article
- Integrin and autocrine IGF2 pathways control fasting insulin secretion in β-cells.The Journal of biological chemistry · 2020Article
- Design, Synthesis, and Biological Evaluation of Proteolysis Targeting Chimeras (PROTACs) for the Dual Degradation of IGF-1R and Src.Molecules (Basel, Switzerland) · 2020Article
- Controlled Signaling-Insulin-Like Growth Factor Receptor Endocytosis and Presence at Intracellular Compartments.Frontiers in endocrinology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IGF-1R expression and activation levels generally cannot be correlated in cancer cells, suggesting that cellular proteins may modulate IGF-1R activity. Strong candidates for such modulation are found in cell-matrix and cell-cell adhesion signaling complexes. Activated IGF-1R is present at focal adhesions, where it can stabilize β1 integrin and participate in signaling complexes that promote invasiveness associated with epithelial mesenchymal transition (EMT) and resistance to therapy. Whether IGF-1R contributes to EMT or to non-invasive tumor growth may be strongly influenced by the degree of extracellular matrix engagement and the presence or absence of key proteins in IGF-1R-cell adhesion complexes. One such protein is PDLIM2, which promotes both cell polarization and EMT by regulating the stability of transcription factors including NFκB, STATs, and beta catenin. PDLIM2 exhibits tumor suppressor activity, but is also highly expressed in certain invasive cancers. It is likely that distinct adhesion complex proteins modulate IGF-1R signaling during cancer progression or adaptive responses to therapy. Thus, identifying the key modulators will be important for developing effective therapeutic strategies and predictive biomarkers.
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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.