Insulin activates EGFR by stimulating its interaction with IGF-1R in low-EGFR-expressing TNBC cells

Miyoung Shin, Eun Gyeong Yang, Hyun Kyu Song, Hyesung Jeon

Research output: Contribution to journalArticle

6 Citations (Scopus)

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-EGFR-expressing 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.

Original languageEnglish
Pages (from-to)342-347
Number of pages6
JournalBMB Reports
Volume48
Issue number6
DOIs
Publication statusPublished - 2015

Keywords

  • EGFR activation
  • IGF-1R interaction
  • Insulin
  • MDA-MB-436
  • Triple-negative breast cancer cells

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

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