B-cell-derived lymphotoxin promotes castration-resistant prostate cancer

Massimo Ammirante, Jun-Li Luo, Sergei Grivennikov, Sergei Nedospasov and Michael Karin ()
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Massimo Ammirante: Laboratory of Gene Regulation and Signal Transduction, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0723, USA
Jun-Li Luo: Scripps Research Institute-Florida, 130 Scripps Way, Jupiter, Florida 33458, USA
Sergei Grivennikov: Laboratory of Gene Regulation and Signal Transduction, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0723, USA
Sergei Nedospasov: Laboratory of Molecular Immunology, Engelhardt Institute of Molecular Biology, 119991, Moscow, Russia
Michael Karin: Laboratory of Gene Regulation and Signal Transduction, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0723, USA

Nature, 2010, vol. 464, issue 7286, 302-305

Abstract: Lymphotoxin's role in prostate cancer progression In the early stages of prostate cancer, cancerous cell growth is dependent on androgens, hence the success of prostatectomy, radiation and androgen-ablating drug therapies. With time, the cancer often develops into an androgen-insensitive, therapy-resistant form with high mortality rates. Work in mouse models of prostate cancer raises the possibility that androgen-ablating therapies may indirectly promote the development of metastatic secondary tumours. Ammirante et al. report that in mice with transgene-induced spontaneous prostate cancer, B-cell infiltration, a component of the natural inflammatory response, activates lymphotoxin release, which stimulates metastasis. In the second model, involving subcutaneous transplantation of an androgen-dependent prostate cancer cell line, it is shown that regression of androgen-deprived primary tumours results in an inflammatory response — and lymphotoxin production. Interfering with the lymphotoxin pathway may therefore offer therapeutic strategies for androgen-independent prostate cancer.

Date: 2010
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DOI: 10.1038/nature08782

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