scholarly journals Enhancement of paclitaxel activity against hormone-refractory prostate cancer cells in vitro and in vivo by quinacrine

1997 ◽  
Vol 75 (11) ◽  
pp. 1593-1600 ◽  
Author(s):  
PL de Souza ◽  
M Castillo ◽  
CE Myers
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Hormone Refractory Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Hormone Refractory

In vitro antitumor effect of hydroxyurea on hormone-refractory prostate cancer cells and its potentiation by phenylbutyrate

1994 ◽  
Vol 5 (3) ◽  
pp. 336-342 ◽  
Author(s):  
William D Figg ◽  
Ronald G Walls ◽  
Michael R Cooper ◽  
Alain Thibault ◽  
Oliver Sartor ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Antitumor Effect ◽  
Hormone Refractory Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Hormone Refractory

Far-infrared rays control prostate cancer cells in vitro and in vivo

2010 ◽  
Vol 5 (2) ◽  
pp. 178-189
Author(s):  
Hiroki Shima ◽  
Shingo Yamamoto ◽  
Jun Qiu ◽  
Mayumi Shincho ◽  
Seiichi Hirota ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Far Infrared ◽  
Human Prostate ◽  
G1 Arrest ◽  
Hormone Refractory Prostate Cancer ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Hormone Refractory

AbstractWe introduce a new effective method to control hormone-refractory prostate cancer cells using an activated rubber/resin form (RB), far-infrared ray (FIR) emitter, with or without sodium butyrate treatment (NaB). The growth of three human prostate cancer cell lines (Du145, PC-3 and LNCaP) was suppressed in vitro and vivo by FIR, and the cells were eradicated with FIR + 3 mM NaB. G1 arrest and apoptotic pathway proteins were induced by FIR with elevated expressions of apoptosis-related transcripts in cDNA microarray. RB reflects and radiates in the wavelengths of about 4 to 25 µm in the FIR that work to suppress the growth of human prostate cancer cells. Accordingly, this technique may be used as a new therapeutic treatment in hormone-refractory prostate cancer.

scholarly journals Acetyl-L-Carnitine downregulates invasion (CXCR4/CXCL12, MMP-9) and angiogenesis (VEGF, CXCL8) pathways in prostate cancer cells: rationale for prevention and interception strategies

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Denisa Baci ◽  
Antonino Bruno ◽  
Caterina Cascini ◽  
Matteo Gallazzi ◽  
Lorenzo Mortara ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Dietary Supplements ◽  
Cell Lines ◽  
Angiogenic Factors ◽  
Migration And Invasion ◽  
Prostate Cancer Cells

Abstract Background Prostate cancer (PCa) is a leading cause of cancer-related death in males worldwide. Exacerbated inflammation and angiogenesis have been largely demonstrated to contribute to PCa progression. Diverse naturally occurring compounds and dietary supplements are endowed with anti-oxidant, anti-inflammatory and anti-angiogenic activities, representing valid compounds to target the aberrant cytokine/chemokine production governing PCa progression and angiogenesis, in a chemopreventive setting. Using mass spectrometry analysis on serum samples of prostate cancer patients, we have previously found higher levels of carnitines in non-cancer individuals, suggesting a protective role. Here we investigated the ability of Acetyl-L-carnitine (ALCAR) to interfere with key functional properties of prostate cancer progression and angiogenesis in vitro and in vivo and identified target molecules modulated by ALCAR. Methods The chemopreventive/angiopreventive activities ALCAR were investigated in vitro on four different prostate cancer (PCa) cell lines (PC-3, DU-145, LNCaP, 22Rv1) and a benign prostatic hyperplasia (BPH) cell line. The effects of ALCAR on the induction of apoptosis and cell cycle arrest were investigated by flow cytometry (FC). Functional analysis of cell adhesion, migration and invasion (Boyden chambers) were performed. ALCAR modulation of surface antigen receptor (chemokines) and intracellular cytokine production was assessed by FC. The release of pro-angiogenic factors was detected by a multiplex immunoassay. The effects of ALCAR on PCa cell growth in vivo was investigated using tumour xenografts. Results We found that ALCAR reduces cell proliferation, induces apoptosis, hinders the production of pro inflammatory cytokines (TNF-α and IFN-γ) and of chemokines CCL2, CXCL12 and receptor CXCR4 involved in the chemotactic axis and impairs the adhesion, migration and invasion capabilities of PCa and BPH cells in vitro. ALCAR exerts angiopreventive activities on PCa by reducing production/release of pro angiogenic factors (VEGF, CXCL8, CCL2, angiogenin) and metalloprotease MMP-9. Exposure of endothelial cells to conditioned media from PCa cells, pre-treated with ALCAR, inhibited the expression of CXCR4, CXCR1, CXCR2 and CCR2 compared to those from untreated cells. Oral administration (drinking water) of ALCAR to mice xenografted with two different PCa cell lines, resulted in reduced tumour cell growth in vivo. Conclusions Our results highlight the capability of ALCAR to down-modulate growth, adhesion, migration and invasion of prostate cancer cells, by reducing the production of several crucial chemokines, cytokines and MMP9. ALCAR is a widely diffused dietary supplements and our findings provide a rational for studying ALCAR as a possible molecule for chemoprevention approaches in subjects at high risk to develop prostate cancer. We propose ALCAR as a new possible “repurposed agent’ for cancer prevention and interception, similar to aspirin, metformin or beta-blockers.

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