Inhibition of Apoptosis by Amphiregulin via an Insulin-like Growth Factor-1 Receptor-Dependent Pathway in Non-Small Cell Lung Cancer Cell Lines

: The reciprocal activation of amphiregulin (AR) and insulin‐like growth factor‐1 (IGF1) pathways has been shown to induce inhibition of serum deprivation apoptosis in non‐small cell lung cancer (NSCLC) cell lines H358 and H322. We demonstrated that AR activated the IGF1 receptor (IGF1‐R), which in...

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Published inAnnals of the New York Academy of Sciences Vol. 1010; no. 1; pp. 354 - 357
Main Authors HURBIN, AMANDINE, DUBREZ, LAURENCE, COLL, JEAN-LUC, FAVROT, MARIE C.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.12.2003
Subjects
Amphiregulin
apoptosis
Apoptosis - drug effects
Apoptosis - physiology
Carcinoma, Non-Small-Cell Lung
Cell Line, Tumor
Culture Media, Serum-Free
EGF Family of Proteins
Glycoproteins - pharmacology
Humans
insulin-like growth factor-1 receptor
Intercellular Signaling Peptides and Proteins - pharmacology
lung cancer
Lung Neoplasms
Receptor, IGF Type 1 - drug effects
Receptor, IGF Type 1 - physiology
serum deprivation
Tyrphostins - pharmacology
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Summary:: The reciprocal activation of amphiregulin (AR) and insulin‐like growth factor‐1 (IGF1) pathways has been shown to induce inhibition of serum deprivation apoptosis in non‐small cell lung cancer (NSCLC) cell lines H358 and H322. We demonstrated that AR activated the IGF1 receptor (IGF1‐R), which in turn induced the secretion of AR and IGF1. Transactivation of the IGF1‐R by AR is independent of its binding to EGFR. Thus, AR can inhibit apoptosis in NSCLC cells through an IGF1‐R‐dependent pathway.
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ISSN:0077-8923
1749-6632
DOI:10.1196/annals.1299.065