ArticleCancer letters2013
IRS1 is highly expressed in localized breast tumors and regulates the sensitivity of breast cancer cells to chemotherapy, while IRS2 is highly expressed in invasive breast tumors.
Article in Cancer letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Pooled it
- Therapeutic delivery of albumin-binding siRNA targeting IRS2 to diverse cell types reduces mammary tumor growth.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Mixed-model and transcriptome-wide association analyses identify transcription factors and genes associated with colorectal cancer susceptibility.Nature communications · 2026Article
- Insights into the molecular and genetic role of obesity in breast cancer pathogenesis.Cancer biology & therapy · 2025Review
- Linking microRNA to metabolic reprogramming and gut microbiota in the pathogenesis of colorectal cancer (Review).International journal of molecular medicine · 2025Review
- Decoding the Role of Insulin-like Growth Factor 1 and Its Isoforms in Breast Cancer.International journal of molecular sciences · 2024Review
- HDAC inhibitors target IRS4 to enhance anti‑AR therapy in AR‑positive triple‑negative breast cancer.International journal of oncology · 2024Article
- The Anticancer Effects of Marine Carotenoid Fucoxanthin through Phosphatidylinositol 3-Kinase (PI3K)-AKT Signaling on Triple-Negative Breast Cancer Cells.Molecules (Basel, Switzerland) · 2023Article
- The Insulin Receptor Substrate 2 Mediates the Action of Insulin on HeLa Cell Migration via the PI3K/Akt Signaling Pathway.Current issues in molecular biology · 2023Article
- The Insulin-like Growth Factor Signaling Pathway in Breast Cancer: An Elusive Therapeutic Target.Life (Basel, Switzerland) · 2022Review
- STAT family of transcription factors in breast cancer: Pathogenesis and therapeutic opportunities and challenges.Seminars in cancer biology · 2022Review
- Article
- Spatiotemporal regulation of insulin signaling by liquid-liquid phase separation.Cell discovery · 2022Article
- Identification of Immune-Related Breast Cancer Chemotherapy Resistance GenesFrontiers in oncology · 2022Article
- MPA alters metabolic phenotype of endometrial cancer-associated fibroblasts from obese women via IRS2 signaling.PloS one · 2022Article
- Epithelial-Mesenchymal Transition-Based Gene Signature and Distinct Molecular Subtypes for Predicting Clinical Outcomes in Breast Cancer.International journal of general medicine · 2022Article
- Network Pharmacology-Based Prediction and Verification of Ginsenoside Rh2-Induced Apoptosis of A549 CellsFrontiers in pharmacology · 2022Article
- IL-4 and IL-13 Promote Proliferation of Mammary Epithelial Cells through STAT6 and IRS-1.International journal of molecular sciences · 2021Article
- Article
- Diversity of insulin and IGF signaling in breast cancer: Implications for therapy.Molecular and cellular endocrinology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Insulin receptor substrate (IRS) proteins have been shown to play an important role in breast cancer by differentially regulating cancer cell survival, proliferation, and motility. Furthermore, the IL-4-induced tyrosine phosphorylation of the transcription factor STAT6 was shown to protect breast cancer cells from apoptosis. Here, we analyzed human breast cancer tissues for the expression of IRS1, IRS2, STAT6, and tyrosine phosphorylated STAT6 (pSTAT6). We found that IRS1 and pSTAT6 were both highly expressed in ductal carcinoma in situ (DCIS). On the other hand, IRS2 expression was low in DCIS, but increased significantly in relation to tumor invasiveness. We utilized cell lines with disparate IRS1 expression, MDA-MB-231, MCF7, and MCF7 cells with depleted IRS1 due to shRNA lentiviral infection, to examine the role of IRS1 and IRS2 in the responsiveness of breast cancer cells to chemotherapy. We report that high IRS1 sensitized MCF7 cells to specific chemotherapeutic agents. These results suggest that high IRS1 with low IRS2 expression may predict the effectiveness of specific types of chemotherapy in breast cancer.
Indexed as
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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.