Skip regulates TGF- β 1-induced extracellular matrix degrading proteases expression in human PC-3 prostate cancer cells
Abstract
Purpose. To determine whether Ski-interacting protein (SKIP) regulates TGF-β1-stimulated expression of urokinase-type plasminogen activator (uPA), matrix metalloproteinase-9 (MMP-9), and uPA Inhibitor (PAI-1) in the androgen-independent human prostate cancer cell model. Materials and Methods. PC-3 prostate cancer cell line was used. The role of SKIP was evaluated using synthetic small interference RNA (siRNA) compounds. The expression of uPA, MMP-9, and PAI-1 was evaluated by zymography assays, RT-PCR, and promoter transactivation analysis. Results. In PC-3 cells TGF-β1 treatment stimulated uPA, PAI-1, and MMP-9 expressions. The knockdown of SKIP in PC-3 cells enhanced the basal level of uPA, and TGF-β1 treatment inhibited uPA production. Both PAI-1 and MMP-9 production levels were increased in response to TGF-β1. The ectopic expression of SKIP inhibited both TGF-β1-induced uPA and MMP-9 promoter transactivation, while PAI-1 promoter response to the factor was unaffected. Conclusions. ...SKIP regulates the expression of uPA, PAI-1, and MMP-9 stimulated by TGF-β1 in PC-3 cells. Thus, SKIP is implicated in the regulation of extracellular matrix degradation and can therefore be suggested as a novel therapeutic target in prostate cancer treatment. © 2013 Victor Villar et al.
Source:
Prostate Cancer, 2013, 2013Publisher:
- Hindawi Limited
Funding / projects:
Collections
Institution/Community
Institut za medicinska istraživanjaTY - JOUR AU - Villar, Victor AU - Kocić, Jelena AU - Santibanez, Juan PY - 2013 UR - http://rimi.imi.bg.ac.rs/handle/123456789/506 AB - Purpose. To determine whether Ski-interacting protein (SKIP) regulates TGF-β1-stimulated expression of urokinase-type plasminogen activator (uPA), matrix metalloproteinase-9 (MMP-9), and uPA Inhibitor (PAI-1) in the androgen-independent human prostate cancer cell model. Materials and Methods. PC-3 prostate cancer cell line was used. The role of SKIP was evaluated using synthetic small interference RNA (siRNA) compounds. The expression of uPA, MMP-9, and PAI-1 was evaluated by zymography assays, RT-PCR, and promoter transactivation analysis. Results. In PC-3 cells TGF-β1 treatment stimulated uPA, PAI-1, and MMP-9 expressions. The knockdown of SKIP in PC-3 cells enhanced the basal level of uPA, and TGF-β1 treatment inhibited uPA production. Both PAI-1 and MMP-9 production levels were increased in response to TGF-β1. The ectopic expression of SKIP inhibited both TGF-β1-induced uPA and MMP-9 promoter transactivation, while PAI-1 promoter response to the factor was unaffected. Conclusions. SKIP regulates the expression of uPA, PAI-1, and MMP-9 stimulated by TGF-β1 in PC-3 cells. Thus, SKIP is implicated in the regulation of extracellular matrix degradation and can therefore be suggested as a novel therapeutic target in prostate cancer treatment. © 2013 Victor Villar et al. PB - Hindawi Limited T2 - Prostate Cancer T1 - Skip regulates TGF- β 1-induced extracellular matrix degrading proteases expression in human PC-3 prostate cancer cells VL - 2013 DO - 10.1155/2013/398253 ER -
@article{ author = "Villar, Victor and Kocić, Jelena and Santibanez, Juan", year = "2013", abstract = "Purpose. To determine whether Ski-interacting protein (SKIP) regulates TGF-β1-stimulated expression of urokinase-type plasminogen activator (uPA), matrix metalloproteinase-9 (MMP-9), and uPA Inhibitor (PAI-1) in the androgen-independent human prostate cancer cell model. Materials and Methods. PC-3 prostate cancer cell line was used. The role of SKIP was evaluated using synthetic small interference RNA (siRNA) compounds. The expression of uPA, MMP-9, and PAI-1 was evaluated by zymography assays, RT-PCR, and promoter transactivation analysis. Results. In PC-3 cells TGF-β1 treatment stimulated uPA, PAI-1, and MMP-9 expressions. The knockdown of SKIP in PC-3 cells enhanced the basal level of uPA, and TGF-β1 treatment inhibited uPA production. Both PAI-1 and MMP-9 production levels were increased in response to TGF-β1. The ectopic expression of SKIP inhibited both TGF-β1-induced uPA and MMP-9 promoter transactivation, while PAI-1 promoter response to the factor was unaffected. Conclusions. SKIP regulates the expression of uPA, PAI-1, and MMP-9 stimulated by TGF-β1 in PC-3 cells. Thus, SKIP is implicated in the regulation of extracellular matrix degradation and can therefore be suggested as a novel therapeutic target in prostate cancer treatment. © 2013 Victor Villar et al.", publisher = "Hindawi Limited", journal = "Prostate Cancer", title = "Skip regulates TGF- β 1-induced extracellular matrix degrading proteases expression in human PC-3 prostate cancer cells", volume = "2013", doi = "10.1155/2013/398253" }
Villar, V., Kocić, J.,& Santibanez, J.. (2013). Skip regulates TGF- β 1-induced extracellular matrix degrading proteases expression in human PC-3 prostate cancer cells. in Prostate Cancer Hindawi Limited., 2013. https://doi.org/10.1155/2013/398253
Villar V, Kocić J, Santibanez J. Skip regulates TGF- β 1-induced extracellular matrix degrading proteases expression in human PC-3 prostate cancer cells. in Prostate Cancer. 2013;2013. doi:10.1155/2013/398253 .
Villar, Victor, Kocić, Jelena, Santibanez, Juan, "Skip regulates TGF- β 1-induced extracellular matrix degrading proteases expression in human PC-3 prostate cancer cells" in Prostate Cancer, 2013 (2013), https://doi.org/10.1155/2013/398253 . .