BCL-2 and BCL-XL expression are down-regulated in benign prostate hyperplasia nodules and not affected by finasteride and/or celecoxib.
BCL-2 and BCL-XL expression are down-regulated in benign prostate hyperplasia nodules and not affected by finasteride and/or celecoxib.
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发表时间：
2018-02
影响因子：
1.2
通讯作者：
Feng Li;Laura E. Pascal;Jianhua Zhou;Yibin Zhou;Ke Wang;A. Parwani;R. Dhir;P. Guo;D. He
中科院分区：
文献类型：
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作者：
Feng Li;Laura E. Pascal;Jianhua Zhou;Yibin Zhou;Ke Wang;A. Parwani;R. Dhir;P. Guo;D. He
良性前列腺增生症（BPH）的发病机制尚不清楚。BPH发病机制中的一个潜在机制可能涉及与细胞凋亡和增殖相关的基因表达的改变，因为细胞死亡减少和增殖增加被认为有助于前列腺肥大。本研究检测了B细胞淋巴瘤2（BCL-2）和超大型B细胞淋巴瘤（BCL-XL）的表达，这两种重要的抗凋亡因子也能够通过加速G1停滞或延迟G1/S转换来抑制细胞增殖，使用免疫染色在来自雄激素操作初治患者的简单前列腺切除术BPH标本中进行。由于雄激素和炎症被认为在BPH发病机制中起重要作用，我们测试了抑制5 α-还原酶和/或考克斯-2对来自患有BPH的前列腺癌患者的BPH样本中BCL-2和BCL-XL表达的影响。这些患者既往未使用过慢性NSAID和/或5 α-还原酶抑制剂，手术前连续28天接受塞来昔布、非那肽、塞来昔布+非那肽治疗或未接受治疗。在所有标本中，BCL-2和BCL-XL染色在腔上皮细胞和基底上皮细胞中均明显，其中基底细胞染色更强烈。与周围正常前列腺组织相比，BPH结节中的管腔细胞和基底细胞均表现出减少的BCL-2和BCL-XL染色。在前列腺癌伴BPH患者中，塞来昔布和/或非那肽对BPH结节和正常邻近组织中的管腔或基底细胞中BCL-2和BCL-XL的表达没有影响。这些结果表明BCL-2和BCL-XL可能在BPH发病机制中起抗增殖因子的作用，塞来昔布和/或非那肽对BPH的作用不太可能通过调节BCL-2和BCL-XL信号传导介导。
The mechanisms involved in the development of benign prostatic hyperplasia (BPH) are poorly understood. One potential mechanism involved in BPH pathogenesis may involve altered expression of genes related to apoptosis and proliferation because reduced cell death and increased proliferation are thought to contribute to prostatic enlargement. This study examined the expression of B-cell lymphoma 2 (BCL-2) and B-cell lymphoma-extra large (BCL-XL), two important anti-apoptosis factors that are also capable of inhibiting cell proliferation via accelerated G1 arrest or delayed G1/S transition, using immunostaining in simple prostatectomy BPH specimens from patients naïve to androgen manipulation. Since androgens and inflammation are thought to play important roles in BPH pathogenesis, we tested the effect of inhibiting 5a-reductase and/or COX-2 on the expression of BCL-2 and BCL-XL in BPH specimens from prostate cancer patients with BPH. These patients had no prior use of chronic NSAIDs and/or 5a-reductase inhibitors and were treated with celecoxib, finasteride, celecoxib plus finasteride or no treatment for 28 consecutive days prior to surgery. In all specimens, BCL-2 and BCL-XL staining was evident in both luminal and basal epithelial cells, with more intense staining in basal cells. Both luminal and basal cells exhibited decreased BCL-2 and BCL-XL staining in BPH nodules compared to the surrounding normal prostatic tissues. In prostate cancer patients with BPH, celecoxib and/or finasteride did not affect the expression of BCL-2 and BCL-XL in luminal or basal cells in BPH nodules and normal adjacent tissues. These results suggest that BCL-2 and BCL-XL may act as anti-proliferative factors in BPH pathogenesis, and the effect of celecoxib and/or finasteride on BPH is unlikely mediated through modulating BCL-2 and BCL-XL signaling.