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Extracellular cleavage of the p75 neurotrophin receptor is implicated in its pro‐survival effect in breast cancer cells
Author(s) -
Verbeke Stéphanie,
Tomellini Elisa,
Dhamani Fatima,
Meignan Samuel,
Adriaenssens Eric,
Xuefen Le Bourhis
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.06.039
Subject(s) - low affinity nerve growth factor receptor , neurotrophin , microbiology and biotechnology , intracellular , cleavage (geology) , receptor , extracellular , apoptosis , biology , cancer cell , kinase , poly adp ribose polymerase , chemistry , cancer , biochemistry , enzyme , genetics , polymerase , paleontology , fracture (geology)
The p75 neurotrophin receptor (p75 NTR ) undergoes sequential proteolytic cleavages leading to the generation of a carboxyl‐terminal fragment (p75 NTR ‐CTF) and an intracellular domain (p75 NTR ‐ICD) in many cellular models. We have previously shown that p75 NTR is involved in the survival of breast cancer cells. Here, we demonstrated that p75 NTR cleavage occurs also in these cells. Surprisingly, p75 NTR ‐CTF increased cell survival, whereas p75 NTR ‐ICD had no effect. The pro‐survival effect of p75 NTR ‐CTF was associated with a decrease of TNF‐related apoptosis‐inducing ligand (TRAIL)‐induced PARP and caspase 3 cleavages. Finally, our findings indicate that p75 NTR could favor cell survival via its carboxyl‐terminal fragment, independently of PI3‐kinase, NF‐κB, or MAP kinase signaling pathways.