探討連翹活性物質Phillyrin藉由AMPK路徑調控攝護腺癌細胞遷移和粒線體生合成
呂政昕1,3,4、王強庭2、謝佩坊3,7、吳俊賢3,5,6、吳振宇3,8、林嘉祥3,8
1部立澎湖醫院泌尿科、2國軍高雄總醫院泌尿科、3義大醫院泌尿科、4義大癌治療醫院泌尿科、5義守大學生物技術與化學工程學系、6義守大學護理學系、7中華醫事科技大學生物醫學保健科、8義守大學醫學系
Phillyrin regulates prostate cancer migration and mitochondrial biogenesis through AMPK pathway
Cheng-Hsin Lu1,3,4, Chiang-Ting Wang2, Pei-Fang Hsieh3,7, Chun-Hsien Wu3,5,6,Chen-Yu Wu3,8, and Victor Chia Hsiang Lin3,8
1Division of Urology, Penghu Hospital; 2Division of Urology, Department of Surgery, Kaohsiung Armed Forces General Hospital; 3Division of Urology, Department of Surgery, E-Da Hospital; 4Division of Urology, Department of Surgery, E-Da Cancer Hospital; Departments of 5Chemical Engineering and Institute of Biotechnology and Chemical Engineering and 6Nursing, I-Shou University; 7Department of Medical Laboratory Science and Biotechnology, Chung-Hwa University of Medical Technology; 8School of Medicine, College of Medicine, I-Shou University, Kaohsiung 824005;
Purpose:
Phillyrin, one of the major components of Forsythia suspensa, has been reported to produce antioxidant, antibacterial, anti-obesity, and anti-inflammatory effects. Our purpose is to find the effect of phyllyrin on prostate cancer and the possible underlying molecular mechanism.
Materials and Methods:
PC-3 cells were purchased from the American Type Culture Collection. To evaluate the effect of Phillyrin on prostate cancer, MTT assay was used to measure cell viability and proliferation. The wound healing assay was used to examine the mobility of PC-3 cells. Western blotting and Immunofluorescence staining were used for protein determination. Each experiment was performed at least three times.
Results:
The human prostate cancer cell lines, PC-3, were treated with various concentrations of Phillyrin(1, 2.5, 5μM). Phillyrin treatment significantly and dose-dependently inhibits PC3 cell viability and proliferation. Phillyrin also had a negative effect on PC3 cell migration. The activity of Mitochondria transcription was increased as the concentration of Phillyrin increased. We also demonstrated that Phillyrin decreased the expression of EMT promotors, Snail and Slug, with increased expression of E-cadherin.
Conclusion:
Phillyrin can inhibit prostate cacner cell proliferation and viability and the effect of suppression was positively correlated with the concentration of Phillyrin. By activating mitochondrial biogenesis and its substream proteins, like AMPK、SIRT1、NRF1, Phillyrin inhibit the migration capacity of prostate cancer cell and EMT.