Wu Chun-Te, Wang Wen-Ching, Chen Miao-Fen, Su Hou-Yu, Chen Wei-Yu, Wu Chih-Hsiung, Chang Yu-Jia, Liu Hui-Hsiung
Chang Gung University College of Medicine and Chang Gung Institute of Technology, Taipei, Taiwan.
Tumour Biol. 2014 Jan;35(1):195-204. doi: 10.1007/s13277-013-1024-4. Epub 2013 Aug 7.
Glucose-regulated protein 78 (GRP78) plays an essential role in embryonic development and in the progression and therapeutic resistance of many cancers. However, little is known about the function of GRP78 in hormone-independent prostate cancer. Here, we found that the expression levels of GRP78 were higher in PC-3 cells than in DU-145 cells. When the expression of GRP78 was silenced using a GRP78-specific small interfering RNA in PC-3 cells, the growth rate and adhesive ability were reduced. Cell migration was dramatically decreased in GRP78-depleted cells. Dissection of the involved signal pathways revealed that maspin expression was upregulated after silencing GRP78 expression. The upregulation of maspin and downregulation of COX-2 may cause the decrease in cell proliferation and migration observed after silencing GRP78 expression. Silencing GRP78 expression may suppress the proliferation, adhesion, and migration of prostate cancer cells via maspin and COX-2 regulation.
葡萄糖调节蛋白78（GRP78）在胚胎发育以及许多癌症的进展和治疗抗性中起着至关重要的作用。然而，关于GRP78在激素非依赖性前列腺癌中的功能却知之甚少。在此，我们发现PC-3细胞中GRP78的表达水平高于DU-145细胞。当在PC-3细胞中使用GRP78特异性小干扰RNA沉默GRP78的表达时，细胞的生长速率和黏附能力降低。GRP78缺失的细胞中细胞迁移显著减少。对相关信号通路的剖析显示，沉默GRP78表达后，maspin表达上调。maspin的上调和COX-2的下调可能导致沉默GRP78表达后观察到的细胞增殖和迁移减少。沉默GRP78表达可能通过调节maspin和COX-2来抑制前列腺癌细胞的增殖、黏附和迁移。
