Li Weiping, Dong Yongchao, Zhang Bin, Kang Yindong, Yang Xukai, Wang He
Department of Urology, Xi'an Tangdu Hospital, the Fourth Military Medical University, Xi'an, Shaanxi 710038, China; Department of Urology, Lanzhou General Hospital of Lanzhou Military Region, Lanzhou, Gansu 730050, China.
Department of Urology, Lanzhou General Hospital of Lanzhou Military Region, Lanzhou, Gansu 730050, China.
Biomed Pharmacother. 2016 Jul;81:1-6. doi: 10.1016/j.biopha.2016.03.030. Epub 2016 Apr 6.
Hypoxia induced epithelial-to-mesenchymal transition (EMT) to facilitate the tumor biology. Phosphatidylethanolamine-binding protein 4 (PEBP4) is a member of the PEBP family and has been reported to be upregulated in various cancer types. The definite function of PEBP4 in regulating the EMT of prostate cancer, however, is still unclear. Here, we examined the functional role of PEBP4 and the underlying molecular mechanisms in hypoxia-induced EMT in prostate cancer cells. Our results showed that PEBP4 mRNA and protein expression was markedly increased in the human prostate cancer tissues and cell lines. Knockdown of PEBP4 significantly inhibited hypoxia-induced migration/invasion and EMT program. Furthermore, knockdown of PEBP4 prevented hypoxia-induced the expression of p-Akt and p-mTOR in prostate cancer cells. Taken together, this study reported here provided evidence that knockdown of PEBP4 inhibited hypoxia-induced EMT in prostate cancer cells. Our study uncovered a novel role for PEBP4 in prostate cancer progression, which might support the potential for PEBP4 targeting in prostate cancer therapy.
缺氧诱导上皮-间质转化(EMT)以促进肿瘤生物学行为。磷脂酰乙醇胺结合蛋白4(PEBP4)是PEBP家族成员,据报道在多种癌症类型中表达上调。然而,PEBP4在调节前列腺癌EMT中的具体功能仍不清楚。在此,我们研究了PEBP4在前列腺癌细胞缺氧诱导的EMT中的功能作用及其潜在分子机制。我们的结果表明,PEBP4 mRNA和蛋白表达在人前列腺癌组织和细胞系中显著增加。敲低PEBP4可显著抑制缺氧诱导的迁移/侵袭及EMT程序。此外,敲低PEBP4可阻止缺氧诱导前列腺癌细胞中p-Akt和p-mTOR的表达。综上所述,本研究提供了证据表明敲低PEBP4可抑制前列腺癌细胞缺氧诱导的EMT。我们的研究揭示了PEBP4在前列腺癌进展中的新作用,这可能支持将PEBP4作为前列腺癌治疗靶点的潜力。