Inhibition of IGF-1R-dependent PI3K activation sensitizes colon cancer cells specifically to DR5-mediated apoptosis but not to rhTRAIL | Zendy

Bodvaël Pennarun | Zendy; Jan H. Kleibeuker | Zendy; Tjitske A. Oenema | Zendy; J.H. Stegehuis | Zendy; Elisabeth G.E. de Vries | Zendy; Steven de Jong | Zendy

Open Access

Inhibition of IGF-1R-dependent PI3K activation sensitizes colon cancer cells specifically to DR5-mediated apoptosis but not to rhTRAIL

Author(s) -

Bodvaël Pennarun,

Jan H. Kleibeuker,

Tjitske A. Oenema,

J.H. Stegehuis,

Elisabeth G.E. de Vries,

Steven de Jong

Publication year - 2011

Publication title -

cellular oncology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.698

H-Index - 40

eISSN - 2211-3436

pISSN - 2211-3428

DOI - 10.1007/s13402-011-0033-9

Subject(s) - apoptosis , pi3k/akt/mtor pathway , caspase 8 , cancer research , ly294002 , tumor necrosis factor alpha , signal transduction , microbiology and biotechnology , biology , receptor , caspase 3 , chemistry , programmed cell death , immunology , biochemistry

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) initiates apoptosis in tumor cells upon binding to its cognate agonistic receptors, death receptors 4 and 5 (DR4 and DR5). The activity of the insulin-like growth factor 1 (IGF-1) survival pathway is often increased in cancer, influencing both cell proliferation and apoptosis. We hypothesized that inhibiting the IGF-1 receptor (IGF-1R) using NVP-AEW541, a small molecular weight tyrosine kinase inhibitor of the IGF-1R, could increase death receptor (DR)-mediated apoptosis in colon cancer cells.

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