Premium
Epidermal growth factor, neurotrophins and the metastatic cascade in prostate cancer
Author(s) -
Montano Ximena,
Djamgoz Mustafa B.A
Publication year - 2004
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.2004.06.088
Subject(s) - paracrine signalling , autocrine signalling , neurotrophin , epidermal growth factor , nerve growth factor , prostate cancer , growth factor , growth factor receptor inhibitor , cancer research , androgen receptor , biology , stromal cell , endocrinology , medicine , receptor tyrosine kinase , epidermal growth factor receptor , intracrine , receptor , microbiology and biotechnology , signal transduction , cancer
Although cancer of the prostate (CaP) is the most commonly occurring cancer in males, there are major limitations in its diagnosis and long‐term cure. Consequently, understanding the molecular mechanisms involved in the progression of CaP is of particular importance for production of pharmacological and biological agents to manage the disease. The development of the normal prostate is regulated by stromal–epithelial interactions via endocrine and paracrine factors, such as androgens and growth factors, which act as precise homeostatic regulators of cellular proliferation. Importantly, after a period of hormonal therapy, CaP shifts from an androgen‐dependent to an androgen‐independent state with a concomitant switch from paracrine to autocrine growth factor stimulation and subsequent upregulation of growth factor expression. Thus, growth factors and their receptors have a pivotal role in CaP. This is emphasized by current evidence obtained from clinical specimens as well as several in vitro and in vivo models strongly suggesting that epidermal growth factor and the neurotrophins (nerve growth factor, brain derived neurotrophin factor, neurotrophin‐3 and neurotrophin‐4/5) together with their tyrosine kinase receptors could play a very significant role in CaP progression.