The impact of altered annexin I protein levels on apoptosis and signal transduction pathways in prostate cancer cells

The Prostate ◽  
2006 ◽  
Vol 66 (13) ◽  
pp. 1413-1424 ◽  
Author(s):  
Chin-Hui Hsiang ◽  
Toshiyuki Tunoda ◽  
Young E. Whang ◽  
Darren R. Tyson ◽  
David K. Ornstein
Keyword(s):  
Prostate Cancer ◽  
Signal Transduction ◽  
Cancer Cells ◽  
Signal Transduction Pathways ◽  
Prostate Cancer Cells ◽  
Protein Levels ◽  
Annexin I ◽  
The Impact

Modulation of Cell-Cycle Regulatory Signaling Network by 2-Methoxyestradiol in Prostate Cancer Cells Is Mediated through Multiple Signal Transduction Pathways†

Biochemistry ◽  
2006 ◽  
Vol 45 (11) ◽  
pp. 3703-3713 ◽  
Author(s):  
Gibanananda Ray ◽  
Gopal Dhar ◽  
Peter J. Van Veldhuizen ◽  
Snigdha Banerjee ◽  
Neela K. Saxena ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Signal Transduction ◽  
Cancer Cells ◽  
Signaling Network ◽  
Signal Transduction Pathways ◽  
Prostate Cancer Cells ◽  
Multiple Signal

Newly synthesized benzimidazoles inhibits vascular endothelial growth factor and matrix metalloproteinase-2 and -9 levels in prostate cancer cells

2021 ◽  
Vol 21 ◽  
Author(s):  
Suleyman Ilhan ◽  
Gamze Dilekci ◽  
Adem Guner ◽  
Hakan Bektas
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Umbilical Vein ◽  
Imidazole Ring ◽  
Matrix Metalloproteinase 2 ◽  
Benzimidazole Derivatives ◽  
Prostate Cancer Cells ◽  
Protein Levels ◽  
Umbilical Vein Endothelial Cells

Background: Investigating the effects of newly synthesized agents on various molecular mechanisms to understand their mechanism of action is an important step of pre-clinical screening. Benzimidazoles are composed of a unique fused benzene and imidazole ring and have attracted great attention due to their broad bioactivities, including antitumor. Objective: In the current study, we reported the synthesis of novel benzimidazole derivatives and investigated the possible cytotoxic and anti-angiogenic effects on human prostate cancer and umbilical vein endothelial cells (HUVECs). Methods: MTT assay was used to assess cell viability. A scratch assay was conducted to monitor the migration of cells. mRNA expression levels of VEGF, MMP-2, and MMP-9 were evaluated using qPCR. Changes in protein levels were evaluated by western blotting. Results: Compound G1, having a chlorine moiety, showed a potent cytotoxic activity on both prostate cancer cells and HUVECs, and inhibited cell migration via decreasing the mRNA and protein levels of key angiogenesis-related molecules such as VEGF, MMP-2, and MMP-9. Conclusion: These results suggest that newly synthesized G1 may be a novel anti-angiogenic agent for prostate cancer treatment.

scholarly journals APE1/Ref-1 redox-specific inhibition decreases survivin protein levels and induces cell cycle arrest in prostate cancer cells

Oncotarget ◽  
2017 ◽  
Vol 9 (13) ◽  
pp. 10962-10977 ◽  
Author(s):  
David W. McIlwain ◽  
Melissa L. Fishel ◽  
Alexander Boos ◽  
Mark R. Kelley ◽  
Travis J. Jerde
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Specific Inhibition ◽  
Prostate Cancer Cells ◽  
Protein Levels ◽  
Survivin Protein ◽  
Cycle Arrest

scholarly journals TGF-β Effects on Prostate Cancer Cell Migration and Invasion Are Mediated by PGE2 through Activation of PI3K/AKT/mTOR Pathway

Endocrinology ◽  
2013 ◽  
Vol 154 (5) ◽  
pp. 1768-1779 ◽  
Author(s):  
BaoHan T. Vo ◽  
Derrick Morton ◽  
Shravan Komaragiri ◽  
Ana C. Millena ◽  
Chelesie Leath ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Mammalian Target Of Rapamycin ◽  
Migration And Invasion ◽  
Prostate Cancer Cells ◽  
Protein Levels ◽  
Prostate Cells ◽  
Pc3 Cells ◽  
Cox 2

Abstract TGF-β plays an important role in the progression of prostate cancer. It exhibits both tumor suppressor and tumor-promoting activities. Correlations between cyclooxygenase (COX)-2 overexpression and enhanced production of prostaglandin (PG)E2 have been implicated in cancer progression; however, there are no studies indicating that TGF-β effects in prostate cancer cells involve PGE2 synthesis. In this study, we investigated TGF-β regulation of COX-1 and COX-2 expression in prostate cancer cells and whether the effects of TGF-β on cell proliferation and migration are mediated by PGE2. COX-1 protein was ubiquitously expressed in prostate cells; however, COX-2 protein levels were detected only in prostate cancer cells. TGF-β treatment increased COX-2 protein levels and PGE2 secretion in PC3 cells. Exogenous PGE2 and PGF2α had no effects on cell proliferation in LNCaP, DU145, and PC3 cells whereas PGE2 and TGF-β induced migration and invasive behavior in PC3 cells. Only EP2 and EP4 receptors were detected at mRNA levels in prostate cells. The EP4-targeting small interfering RNA inhibited PGE2 and TGF-β-induced migration of PC3 cells. TGF-β and PGE2 induce activation of PI3K/AKT/mammalian target of rapamycin pathway as indicated by increased AKT, p70S6K, and S6 phosphorylation. Rapamycin completely blocked the effects of TGF-β and PGE2 on phosphorylation of p70S6K and S6 but not on AKT phosphorylation. PGE2 and TGF-β induced phosphorylation of AKT, which was blocked by antagonists of PGE2 (EP4) receptors (L161982, AH23848) and PI3K inhibitor (LY294002) in PC3 cells. Pretreatment with L161982 or AH23848 blocked the stimulatory effects of PGE2 and TGF-β on cell migration, whereas LY294002 or rapamycin completely eliminated PGE2, TGF-β, and epidermal growth factor-induced migration in PC3 cells. We conclude that TGF-β increases COX-2 levels and PGE2 secretion in prostate cancer cells which, in turn, mediate TGF-β effects on cell migration and invasion through the activation of PI3K/AKT/mammalian target of rapamycin pathway.

Sign in / Sign up

Export Citation Format

Share Document