Functional analysis of KIT-positeive interstitial cells for novel strategies of molecular target therapies for benign prostatic hyperplasia

我们研究kit介导的机制在良性前列腺增生（BPH）中的作用，并讨论BPH的病理生理和BPH药物治疗的候选靶点。KIT在PrSC和人前列腺中均有表达，说明这些样本适合检测KIT的功能。免疫组织化学分析表明，KIT定位于人前列腺基质成分的间质细胞（ICs）。甲磺酸伊马替尼剂量依赖性地抑制PrSC细胞增殖，下调JAK2和STAT1，这是SCF/KIT信号下游的主要途径。SCF通过上调JAK2和STAT1促进PrSC细胞增殖。前列腺增生组织中KIT的表达和KIT阳性ic的数量明显大于正常前列腺组织。

We investigated the role of the KIT-mediated mechanism in benign prostatic hyperplasia (BPH), and discuss the pathophysiology of BPH and a candidate target of BPH medical therapy.KIT was expressed in PrSC and human prostate, indicating that these samples are suitable for examining the function of KIT.Immunohistochemical analysis demonstrated that KIT was localized in interstitial cells (ICs) of the stromal component in human prostate. Administration of imatinib mesylate dose-dependently inhibited cell proliferation of PrSC with downregulation of JAK2 and STAT1, which are the main pathways downstream of SCF/KIT signal. SCF promoted cell proliferation of PrSC with upregulation of JAK2 and STAT1. KIT expression and the number of KIT-positive ICs in BPH were found to be significantly larger than in normal prostate.