4.6 Article

A role for the dehydrogenase DHRS7 (SDR34C1) in prostate cancer

期刊

CANCER MEDICINE
卷 4, 期 11, 页码 1717-1729

出版社

WILEY
DOI: 10.1002/cam4.517

关键词

DHRS7; gene expression; proliferation; prostate cancer; SDR34C1; tumor suppressor

类别

资金

  1. Swiss National Science Foundation [31003A-159454]
  2. International Fellowship Programme on Integrative Kidney Physiology and Pathophysiology
  3. 7th Framework Programme (FP7) of European Commission
  4. Swiss National Centre of Competence in Research (NCCR) Kidney Control of Homeostasis
  5. Swiss National Science Foundation (SNF) [31003A_159454] Funding Source: Swiss National Science Foundation (SNF)

向作者/读者索取更多资源

Several microarray studies of prostate cancer (PCa) samples have suggested altered expression of the orphan enzyme short-chain dehydrogenase/reductase DHRS7 (retSDR4, SDR34C1). However, the role of DHRS7 in PCa is largely unknown and the impact of DHRS7 modulation on cancer cell properties has not yet been studied. Here, we investigated DHRS7 expression in normal humanprostate and PCa tissue samples at different tumor grade using tissue microarray and immunovisualization. Moreover, we characterized the effects of siRNA-mediated DHRS7 knockdown on the properties of three distinct human prostate cell lines. We found that DHRS7 protein expression decreases alongside tumor grade, as judged by the Gleason level, in PCa tissue samples. The siRNA-mediated knockdown of DHRS7 expression in the human PCa cell lines LNCaP, BPH1, and PC3 significantly increased cell proliferation in LNCaP cells as well as cell migration in all of the investigated cell lines. Furthermore, cell adhesion was decreased upon DHRS7 knockdown in all three cell lines. To begin to understand the mechanisms underlying the effects of DHRS7 depletion, we performed a microarray study with samples from LNCaP cells treated with DHRS7-specific siRNA. Several genes involved in cell proliferation and adhesion pathways were found to be altered in DHRS7-depleted LNCaP cells. Additionally, genes of the BRCA1/2 pathway and the epithelial to mesenchymal transition regulator E-cadherin were altered following DHRS7 knockdown. Based on these results, further research is needed to evaluate the potential role of DHRS7 as a tumor suppressor and whether its loss-of-function promotes PCa progression and metastasis.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据