|
|||||
|
|
Glucose-regulated protein 78 mediates hormone-independent prostate cancer progression and metastasis through maspin and COX-2 expression |
|
| Authors: | Chun-Te Wu Wen-Ching Wang Miao-Fen Chen Hou-Yu Su Wei-Yu Chen Chih-Hsiung Wu Yu-Jia Chang Hui-Hsiung Liu |
| Institution: | 1. Chang Gung University College of Medicine and Chang Gung Institute of Technology, Taipei, Taiwan 2. Department of Urology, Chang Gung Memorial Hospital at Keelung, Keelung, Taiwan 3. Department of General Surgery, Chi-Mei Medical Center, Tainan, Taiwan 4. Department of Radiation Oncology, Chang Gung Memorial Hospital, Chiayi, Taiwan 5. Department of Surgery, Saint Mary’s Hospital Luodong Yilan County, Yilan, Taiwan 6. Department of Pathology, Wan-Fang Hospital and Taipei Medical University, Taipei, Taiwan 10. Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan 7. Graduate Institute of Clinical Medicine, College of Medicine Taipei Medical University, Taipei, Taiwan 8. Department of Surgery, Taipei Medical University, Taipei, Taiwan 9. Division of General Surgery, Taipei Medical University and Hospital, Taipei, Taiwan 11. Cancer Research Center, Taipei Medical University and Hospital, Taipei, Taiwan 12. Center of Excellence for Cancer Research, Taipei Medical University, 250 Wu-Xin Street, Taipei, Taiwan, 110 13. Department of Public Health, School of Public Health, Taipei Medical University, 250 Wu-Xin Street, Taipei, Taiwan, 110 |
| Abstract: | 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. |
| Keywords: | |
| 本文献已被 SpringerLink 等数据库收录！ | |