ArticleBritish journal of cancer2006
Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells.
Article in British journal of cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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
66 citing papers in PubMed, 118 citations in OpenAlex.
- Interaction of IRS2 with PLK1 protects cells from mitotic stress.Cell death & disease · 2026Article
- Microproteomic-Based Analysis of the Goat Milk Protein Synthesis Network and Casein Production Evaluation.Foods (Basel, Switzerland) · 2024Article
- IGF-1R targeting in cancer - does sub-cellular localization matter?Journal of experimental & clinical cancer research : CR · 2023Review
- Suppression of Insulin Receptor Substrate 1 Inhibits Breast Cancer Growth In Vitro and in Female Athymic Mice.Endocrinology · 2023Article
- The Insulin-like Growth Factor Signaling Pathway in Breast Cancer: An Elusive Therapeutic Target.Life (Basel, Switzerland) · 2022Review
- Article
- The regulation of adipocyte growth in white adipose tissue.Frontiers in cell and developmental biology · 2022Review
- Visualization of the protein-protein interactions of hormone receptors in hormone-dependent cancer research.Endocrine oncology (Bristol, England) · 2022Review
- Diversity of insulin and IGF signaling in breast cancer: Implications for therapy.Molecular and cellular endocrinology · 2021Review
- Insulin receptor substrate-1 (IRS-1) mediates progesterone receptor-driven stemness and endocrine resistance in oestrogen receptor+ breast cancer.British journal of cancer · 2021Article
- Diarylpentanoid (1,5-bis(4-hydroxy-3-methoxyphenyl)-1,4-pentadiene-3-one) (MS13) Exhibits Anti-proliferative, Apoptosis Induction and Anti-migration Properties on Androgen-independent Human Prostate Cancer by Targeting Cell Cycle-Apoptosis and PI3K Signalling Pathways.Frontiers in pharmacology · 2021Article
- Insulin Receptor Substrate Suppression by the Tyrphostin NT157 Inhibits Responses to Insulin-Like Growth Factor-I and Insulin in Breast Cancer Cells.Hormones & cancer · 2018Article
- Metastatic and triple-negative breast cancer: challenges and treatment options.Drug delivery and translational research · 2018Review
- Association of IRS2 overexpression with disease progression in intrahepatic cholangiocarcinoma.Oncology letters · 2018Article
- Identification of a Novel Invasion-Promoting Region in Insulin Receptor Substrate 2.Molecular and cellular biology · 2018Article
- IL-4 and IL-13 Receptor Signaling From 4PS to Insulin Receptor Substrate 2: There and Back Again, a Historical View.Frontiers in immunology · 2018Review
- Targeting Insulin Receptor in Breast Cancer Using Small Engineered Protein Scaffolds.Molecular cancer therapeutics · 2017Article
- Differential involvement of the microtubule cytoskeleton in insulin receptor substrate 1 (IRS-1) and IRS-2 signaling to AKT determines the response to microtubule disruption in breast carcinoma cells.The Journal of biological chemistry · 2017Article
- Revisiting the IGF-1R as a breast cancer target.NPJ precision oncology · 2017Article
- TGFβ/Smad3 regulates proliferation and apoptosis through IRS-1 inhibition in colon cancer cells.PloS one · 2017Article
6 more citing papers are in PubMed but not listed here.
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 4 institutions in 1 country.
Funding
Abstract
Activation of the type I insulin-like growth factor receptor (IGF-IR) regulates several aspects of the malignant phenotype, including cancer cell proliferation and metastasis. Phosphorylation of adaptor proteins downstream of IGF-IR may couple IGF action to specific cancer phenotypes. In this study, we sought to determine if insulin receptor substrate-1 and -2 (IRS-1 and -2) mediate distinct biological effects in breast cancer cells. Insulin receptor substrate-1 and IRS-2 were expressed in T47D-YA breast cancer cells, which lack IRS-1 and -2 expression, yet retain functional IGF-IR. In the absence of IRS-1 and -2 expression, IGF-IR activation was unable to stimulate proliferation or motility in T47D-YA cells. Expression of IRS-1 resulted in IGF-I-stimulated proliferation, but did not affect motility. In contrast, expression of IRS-2 enhanced IGF-I-stimulated motility, but did not stimulate proliferation. The alphaIR-3, an inhibitor of the IGF-IR, was unable to affect these IGF-stimulated phenotypes unless IRS-1 or -2 was expressed. Thus, IGF-IR alone is unable to regulate important breast cancer cell phenotypes. In these cells, IRS proteins are required for and mediate distinct aspects of IGF-IR-stimulated behaviour. As multiple agents targeting the IGF-IR are currently in early clinical trials, IRS expression should be considered as a potential biomarker for IGF-IR responsiveness.
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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.