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

作者: Julia K. Seibert , Luca Quagliata , Cristina Quintavalle , Thomas G. Hammond , Luigi Terracciano

DOI: 10.1002/CAM4.517

关键词: Tissue microarrayEpithelial–mesenchymal transitionCancer cellGene knockdownCell cultureLNCaPMolecular biologyCell growthCell adhesionCancer researchBiology

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

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