Neurotensin is an autocrine trophic factor stimulated by androgen withdrawal in human prostate cancer
- Inder Sehgal,
- Stephen Powers,
- Brenda Huntley,
- Garth Powis,
- Mark Pittelkow,
- Nita J. Maihle(corresponding author)
- Mayo Clinic College of Medicine and Science,
- ImmuLogic Pharmaceutical Corporation,
- Mayo Clinic Rochester, MN,
- University of Arizona
Open access
Sustainable Development Goals
- SDG 3 Good Health and Well
Abstract
After therapeutic hormone deprivation, prostate cancer cells often develop androgen-insensitive growth through mechanisms thus far undefined. Neuropeptides have been previously implicated as growth factors in some prostate cancers. Here, we demonstrate that androgen-sensitive LNCaP human prostate cancer cells produce and secrete neurotensin following androgen withdrawal. We show that while LNCaP cells express the neurotensin receptor, only androgen-deprived cells exhibit a growth response to exogenous neurotensin. We further demonstrate that androgen-stimulated cells may be refractory to exogenous neurotensin due to androgen induction of a metalloprotease active toward neurotensin. Thus, prostate cancer cells deprived of androgen develop an alternative autocrine growth mechanism involving neurotensin.
Publication Information
Output type
Original language
English (US)Pages from-to (Number of pages)
Pages 4673-4677 (5 pages)Journal (Volume, Issue Number)
Proceedings of the National Academy of Sciences of the United States of America (Volume 91, Issue 11)Publication milestones
- Published - 05/24/1994
Publication status
ISSN
0027-8424Publication IDs
- Scopus: 0028290656
- PubMed: 8197117
