Increased Migration Inhibitory Factor (MIF) Secretion By Neuroendocrine Differentiated LNCaP Cells Induces Proliferation Of Prostate Cancer

Main Category: Prostate / Prostate Cancer
Also Included In: Urology / Nephrology;  Men's health
Article Date: 20 Apr 2008 - 0:00 PDT

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UroToday.com - The poster presented data regarding macrophage migration inhibitory factor (MIF), initially identified as a pro-inflammatory cytokine expressed at baseline in numerous cell types and tissues.

MIF has also been implicated in processes associated with tumor survival, including cell division and survival, angiogenesis and suppression of host-tumor cell immune surveillance. In CaP, MIF serum value mirrors the extent and the aggressiveness of the cancer. The investigators used a model of neuroendocrine transdifferentiation of LNCaP cells (initiated by increasing the intracellular levels of cAMP). They report that spontaneous MIF secretion, measured by ELISA, was strongly increased. In contrast, the expression levels of MIF mRNA and intracellular MIF, assessed respectively by Northern and Western blot analyses, were decreased, suggesting that MIF expression is associated with epithelial phenotype. A 1201 bp fragment from the human MIF gene cloned in front of the luciferase gene reporter revealed a decreased MIF promoter activity during NE transdifferentiation of LNCaP. In a cell culture system, addition of exogenous MIF to different prostate cancer cell lines stimulated cell proliferation and decreased Paclitaxel- and Thapsigargin induced cell apoptosis. However, the data did not investigate whether MIF supports androgen independent growth of LNCaP. The presenter stated that the effect is paracrine, but the data would more likely support that it is autocrine.

Presented by: Tawadros T., Roger T., Calandra T., Haefliger J.A., Jichlinski P. at the European Association of Urology - 23rd Annual EAU Congress - March 26 - 29, 2008 - Milan, Italy

Reported by UroToday.com Contributing Editor Christopher P. Evans, MD, FACS

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