ArticleBMB reports2015
Insulin activates EGFR by stimulating its interaction with IGF-1R in low-EGFR-expressing TNBC cells.
Article in BMB reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Cross-Talk between NOK and EGFR: Juxtamembrane and Kinase domain interactions enhancing STAT3/5 signaling in breast cancer tumorigenesis.Translational oncology · 2025Article
- EGFR Status by Immunohistochemistry in Triple-Negative Breast Cancer: An Evaluation of Prevalence and Association with Clinical and Pathological Parameters.Iranian journal of pathology · 2025Article
- RAGE inhibition blunts insulin-induced oncogenic signals in breast cancer.Breast cancer research : BCR · 2023Article
- Podocyte EGFR Inhibits Autophagy Through Upregulation of Rubicon in Type 2 Diabetic Nephropathy.Diabetes · 2021Article
- 21-Benzylidene digoxin decreases proliferation by inhibiting the EGFR/ERK signaling pathway and induces apoptosis in HeLa cells.Steroids · 2020Article
- EGFR/ErbB Inhibition Promotes OPC Maturation up to Axon Engagement by Co-Regulating PIP2 and MBP.Cells · 2019Article
- An investigation of the equine epidermal growth factor system during hyperinsulinemic laminitis.PloS one · 2019Article
- Akt regulates neurite growth by phosphorylation-dependent inhibition of radixin proteasomal degradation.Scientific reports · 2018Article
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of epidermal growth factor receptor (EGFR) is an important diagnostic marker for triple-negative breast cancer (TNBC) cells, which lack three hormonal receptors: estrogen and progesterone receptors as well as epidermal growth factor receptor 2. EGFR transactivation can cause drug resistance in many cancers including TNBC, but the mechanism underlying this phenomenon is poorly defined. Here, we demonstrate that insulin treatment induces EGFR activation by stimulating the interaction of EGFR with insulin-like growth factor receptor 1 (IGF-1R) in the MDA-MB-436 TNBC cell line. These cells express low levels of EGFR, while exhibiting high levels of IGF-1R expression and phosphorylation. Low-EGFRexpressing MDA-MB-436 cells show high sensitivity to insulinstimulated cell growth. Therefore, unexpectedly, insulin stimulation induced EGFR transactivation by regulating its interaction with IGF-1R in low-EGFR-expressing TNBC cells.
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