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. 2011 Feb 1;3(1):510–530. doi: 10.3390/cancers3010510

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© 2011 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).

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Figure 2. — Nerve growth factor (NGF) signaling in breast cancer cells. NGF mediated autocrine signaling in breast cancer cells is carried out by two independent signaling pathways via TrkA and p75^NTR. TrkA signals downstream to Ras/MAPK promoting proliferation of cells, as well as invasion and metastasis. p75^NTR signaling results in activation of the transcription factor NF-κB p50/p65 canonical pathway. The precise mechanism leading to NF-κB activation is not fully understood but is known to include TRADD and BEX2. This activation of NF-κB has been shown to be antagonized by the small peptide inhibitor SN-50. Activation of these pathways ultimately results in changes at transcriptional level. PI3K, Phosphatidylinositol-3-kinase; MAPK, Mitogen activated protein kinase; NF-κB, Nuclear factor-κB; IκB Inhibitor of κB; TRADD, Tumor necrosis factor receptor-associated death domain; BEX2, Brain expressed X-linked 2; DD, death domain; Ub, ubiquitin; P, Phosphate.