Inhibition of cell proliferation, invasion, tumor growth and metastasis by an oral non-antimicrobial tetracycline analog (COL-3) in a metastatic prostate cancer model

2002 ◽  
Vol 98 (2) ◽  
pp. 297-309 ◽  
Author(s):  
Bal L. Lokeshwar ◽  
Marie G. Selzer ◽  
Bao-Qian Zhu ◽  
Norman L. Block ◽  
Lorne M. Golub
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Metastatic Prostate Cancer ◽  
Cancer Model ◽  
Tumor Growth And Metastasis ◽  
Prostate Cancer Model

scholarly journals Tumor growth and metastasis suppression by Glipr1 gene-modified macrophages in a metastatic prostate cancer model

Gene Therapy ◽  
2011 ◽  
Vol 18 (10) ◽  
pp. 969-978 ◽  
Author(s):  
K Tabata ◽  
S Kurosaka ◽  
M Watanabe ◽  
K Edamura ◽  
T Satoh ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Growth ◽  
Metastatic Prostate Cancer ◽  
Cancer Model ◽  
Metastasis Suppression ◽  
Tumor Growth And Metastasis ◽  
Prostate Cancer Model

scholarly journals Adenovirus-mediated REIC/Dkk-3 gene transfer inhibits tumor growth and metastasis in an orthotopic prostate cancer model

2007 ◽  
Vol 14 (9) ◽  
pp. 765-772 ◽  
Author(s):  
K Edamura ◽  
Y Nasu ◽  
M Takaishi ◽  
T Kobayashi ◽  
F Abarzua ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Gene Transfer ◽  
Tumor Growth ◽  
Cancer Model ◽  
Tumor Growth And Metastasis ◽  
Prostate Cancer Model

Soy isoflavones enhance radiotherapy in a metastatic prostate cancer model

2007 ◽  
Vol 120 (11) ◽  
pp. 2491-2498 ◽  
Author(s):  
Julian J. Raffoul ◽  
Sanjeev Banerjee ◽  
Mingxin Che ◽  
Zvi E. Knoll ◽  
Daniel R. Doerge ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Metastatic Prostate Cancer ◽  
Soy Isoflavones ◽  
Cancer Model ◽  
Prostate Cancer Model

scholarly journals An orthotopic metastatic prostate cancer model in SCID mice via grafting of a transplantable human prostate tumor line

2005 ◽  
Vol 85 (11) ◽  
pp. 1392-1404 ◽  
Author(s):  
Yuwei Wang ◽  
Hui Xue ◽  
Jean-Claude Cutz ◽  
Jane Bayani ◽  
Nasrin R Mawji ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Metastatic Prostate Cancer ◽  
Scid Mice ◽  
Prostate Tumor ◽  
Human Prostate ◽  
Cancer Model ◽  
Tumor Line ◽  
Human Prostate Tumor ◽  
Prostate Cancer Model

scholarly journals MAZ51 Blocks the Tumor Growth of Prostate Cancer by Inhibiting Vascular Endothelial Growth Factor Receptor 3

2021 ◽  
Vol 12 ◽  
Author(s):  
Aya Yamamura ◽  
Md Junayed Nayeem ◽  
Hiroyuki Muramatsu ◽  
Kogenta Nakamura ◽  
Motohiko Sato
Keyword(s):  
Prostate Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Tumor Growth ◽  
Metastatic Prostate Cancer ◽  
Vascular Endothelial ◽  
Du145 Cells ◽  
Endothelial Growth Factor ◽  
Androgen Independent

Vascular endothelial growth factor (VEGF) signaling plays a critical role in the carcinogenesis and tumor development of several cancer types. However, its pathological significance in prostate cancer, one of the most frequent and lethal malignancies in men, remains unclear. In the present study, we focused on a pathological role of the VEGF receptors (VEGFRs), and examined their expression and effects of MAZ51 (an inhibitor of the tyrosine kinase of VEGFR-3) on cell proliferation, migration, and tumor growth in human prostate cancer cells. The expression level of VEGFR-3 was higher in androgen-independent and highly metastatic prostate cancer PC-3 cells than in other prostate PrEC, LNCaP, and DU145 cells. In PC-3 cells, VEGFR-3 and Akt were phosphorylated following a stimulation with 50 ng/ml VEGF-C, and these phosphorylations were blocked by 3 μM MAZ51. Interestingly, PC-3 cells themselves secreted VEGF-C, which was markedly larger amount compared with PrEC, LNCaP, and DU145 cells. MAZ51 reduced the expression of VEGFR-3 but not VEGFR-1 and VEGFR-2. The proliferation of PC-3 cells was inhibited by MAZ51 (IC50 = 2.7 μM) and VEGFR-3 siRNA, and partly decreased by 100 nM GSK690693 (an Akt inhibitor) and 300 nM VEGFR2 Kinase Inhibitor I. MAZ51 and VEGFR-3 siRNA also attenuated the VEGF-C-induced migration of PC-3 cells. Moreover, MAZ51 blocked the tumor growth of PC-3 cells in a xenograft mouse model. These results suggest that VEGFR-3 signaling contributes to the cell proliferation, migration, and tumor growth of androgen-independent/highly metastatic prostate cancer. Therefore, the inhibition of VEGFR-3 has potential as a novel therapeutic target for the treatment for prostate cancer.

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