CXCR6 Induces Prostate Cancer Progression by the AKT/Mammalian Target of Rapamycin Signaling Pathway

摘要: Previous studies show that the chemokine CXCL16 and its receptor CXCR6 are likely to contribute prostate cancer (PCa). In this investigation, role of in PCa was further explored. protein expression examined using high-density tissue microarrays immunohistochemistry. Expression showed strong epithelial staining correlated with Gleason score. vitro vivo cell lines suggested alterations were associated invasive activities tumor growth. addition, able regulate proangiogenic factors interleukin (IL)-8 or vascular endothelial growth factor (VEGF), which participate regulation angiogenesis. Finally, we found signaling induced activation Akt, p70S6K, eukaryotic initiation 4E binding 1 included mammalian target rapamycin (mTOR) pathways, located downstream Akt. Furthermore, not only drastically inhibited CXCL16-induced invasion but reduced secretion IL-8 VEGF levels other targets including CD44 matrix metalloproteinase 3 cells. Together, our data shows for first time CXCR6/AKT/mTOR pathway plays a central development PCa. Blocking may prove beneficial prevent metastasis provide more effective therapeutic strategy [Cancer Res 2008;68(24):10367–76]