New Modes of GPCR Signalling

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pathways, and the change of signal molecules after the intervention of scorpion polypeptides. Key Words: EAE , Kv1.3 channel, T cells, signaling pathways Acknowledgment: This work was supported by Program for New Century Excellent Talents, Wuhan University (No. NCET-07-0630),the Scientific Research Foundation for the Returned Overseas Chinese Scholars in State Education Ministry, and Research Fund for the Doctoral Program of Higher Education of China (No. 20090141110010). *Corresponding author E-mail: hexiaohua@whu.edu.cn or liwxlab@whu.edu.cn
IGF-1 Promote BPH-1 Cell Proliferation Primarily via Activating mTOR-dependent Translational Increases in Cyclin D Proteins Ke Gong, Chao Chen and Wenhua Li* Department of Cell Biology, College of Life Sciences, Wuhan University, Wuhan 430072, PR China. Aim: Insulin-like growth factor-1 (IGF-1) and its binding protein (IGFBP-3) play a crucial role in the initiation and progression of prostate and benign prostatic hyperplasia (BPH). We have previously report that stromally expressed c-Jun protein modulates the epithelial proliferation via regulating production and paracrine signals of IGF-1, which promote the BPH-1 cells proliferation through upregulate cyclin D protein levels. Methods: Western blots analyses for protein levels and cell cycle array of FACS were performed. Results: In this study, the exact molecular mechanisms of these regulations were investigated. We found that IGF-1 increases cyclin D proteins and promotes cell cycle transition from G0 to S phase, bringing in cell proliferation. IGF-1 almost didn’t affects cyclin D mRNA levels and it primarily stimulates post-transcriptional increases in cyclin D proteins. IGF-1 stimulation increases cyclin D protein in translation levels via activation mammalian target of rapamycin (mTOR) pathway in BPH-1 cells. Two vital factors of mTOR-downstream, the eukaryotic translation initiation factor-4E binding protein-1 (4EBP1) and 70-kD ribosomal protein S6 kinase (p70S6K), were activated after IGF-1 treatment. Blocking mTOR will decrease cyclin D levels and offset IGF-1 stimulation. Moreover, we found that, in BPH-1cells, activated mTOR by IGF-1 increases cyclin D protein expression is mediated through activation of the PI3K/Akt pathways cells, but not MAP kinase pathway. Also, our data indicate that IGF-1 probably influences the combination of cyclin D and ubiquitin, and then stabilize the cyclin D protein. Conclution: These results elucidate the molecular transduction pathways of IGF-1 promote BPH-1 cell proliferation, which will be help to improve our understanding of BPH and develop new clinical therapy for it. Key Words: IGF-1; BPH; mTOR; cyclinD *Corresponding Authors: Wenhua Li, Email: whli@whu.wdu.cn, Tel: 86-27-68756711
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