Role of macrophages in circulating prostate cancer cells studied by in vivo flow cytometry

2013 ◽  
Author(s):  
Rongrong Liu ◽  
Jin Guo ◽  
Zhengqin Gu ◽  
Xunbin Wei
Keyword(s):  
Prostate Cancer ◽  
Flow Cytometry ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
In Vivo Flow Cytometry

STUDYING THE ROLE OF MACROPHAGES IN CIRCULATING PROSTATE CANCER CELLS BY IN VIVO FLOW CYTOMETRY

2012 ◽  
Vol 05 (04) ◽  
pp. 1250027 ◽  
Author(s):  
JIN GUO ◽  
ZHICHAO FAN ◽  
ZHENGQIN GU ◽  
XUNBIN WEI
Keyword(s):  
Prostate Cancer ◽  
Flow Cytometry ◽  
Cancer Cells ◽  
The Body ◽  
Prostate Cancer Cells ◽  
In Vivo Flow Cytometry ◽  
Kinetics Of ◽  
Deficient Group

Metastasis is a very complicated multi-step process and accounts for the low survival rate of the cancerous patients. To metastasize, the malignant cells must detach from the primary tumor and migrate to secondary sites in the body through either blood or lymph circulation. Macrophages appear to be directly involved in tumor progression and metastasis. However, the role of macrophages in affecting cancer metastasis has not been fully elucidated. Here, we have utilized an emerging technique, namely in vivo flow cytometry (IVFC) to study the depletion kinetics of circulating prostate cancer cells in mice and determine how depletion of macrophages by the liposome-encapsulated clodronate affects the depletion kinetics. Our results show different depletion kinetics of PC-3 cells between the macrophage-deficient group and the control group. The number of circulating tumor cells (CTCs) in the macrophage-deficient group decreases in a slower manner compared to the control mice group. The differences in depletion kinetics indicate that the absence of macrophages facilitates the stay of prostate cancer cells in circulation. In addition, our imaging data suggest that macrophages might be able to arrest, phagocytose and digest PC-3 cells. Therefore, phagocytosis may mainly contribute to the depletion kinetic differences. The developed methods elaborated here would be useful to study the relationship between macrophages and tumor metastasis in small animal cancer models.

scholarly journals Role of OATP transporters in steroid uptake by prostate cancer cells in vivo

2016 ◽  
Vol 20 (1) ◽  
pp. 20-27 ◽  
Author(s):  
S M Green ◽  
A Kaipainen ◽  
K Bullock ◽  
A Zhang ◽  
J M Lucas ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells

The Role of Vascular Endothelial Growth Factor in the Tissue Specific in Vivo Growth of Prostate Cancer Cells

2001 ◽  
Vol 18 (4) ◽  
pp. 287-302 ◽  
Author(s):  
Tracey Krupski ◽  
Michael A. Harding ◽  
Michael E. Herce ◽  
Kay M. Gulding ◽  
Mark H. Stoler ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Vascular Endothelial ◽  
Prostate Cancer Cells ◽  
In Vivo Growth ◽  
Endothelial Growth Factor

scholarly journals Roles of the Na+/H+ Exchanger Isoform 1 and Urokinase in Prostate Cancer Cell Migration and Invasion

2021 ◽  
Vol 22 (24) ◽  
pp. 13263
Author(s):  
Xiuju Li ◽  
Benjamin Buckley ◽  
Konstantin Stoletov ◽  
Yang Jing ◽  
Marie Ranson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Colony Formation ◽  
Prostate Cancer Cell ◽  
Cancer Cell Migration ◽  
Prostate Cancer Cells

Prostate cancer is a leading cause of cancer-associated deaths in men over 60 years of age. Most patients are killed by tumor metastasis. Recent evidence has implicated a role of the tumor microenvironment and urokinase plasminogen activator (uPA) in cancer cell migration, invasion, and metastasis. Here, we examine the role of the Na+/H+ exchanger isoform 1 (NHE1) and uPA in DU 145 prostate cancer cell migration and colony formation. Knockout of NHE1 reduced cell migration. The effects of a series of novel NHE1/uPA hexamethylene-amiloride-based inhibitors with varying efficacy towards NHE1 and uPA were examined on prostate cancer cells. Inhibition of NHE1—alone, or with inhibitors combining NHE1 or uPA inhibition—generally did not prevent prostate cancer cell migration. However, uPA inhibition—but not NHE1 inhibition—prevented anchorage-dependent colony formation. Application of inhibitors at concentrations that only saturate uPA inhibition decreased tumor invasion in vivo. The results suggest that while knockout of NHE1 affects cell migration, these effects are not due to NHE1-dependent proton translocation. Additionally, while neither NHE1 nor uPA activity was critical in cell migration, only uPA activity appeared to be critical in anchorage-dependent colony formation of DU 145 prostate cancer cells and invasion in vivo.

scholarly journals l-Cysteine-mediated modulation of copper trafficking in prostate cancer cells: an in vitro and in vivo investigation with 64Cu and 64Cu-PET

Metallomics ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 1508-1520
Author(s):  
Joanna J. Bartnicka ◽  
Fahad Al-salemee ◽  
George Firth ◽  
Philip J. Blower
Keyword(s):  
Prostate Cancer ◽  
Amino Acids ◽  
Cancer Cells ◽  
Whole Body ◽  
Prostate Cancer Cells ◽  
Copper Trafficking ◽  
Body Level

This article reports a novel role of thiol amino acids in modulating intracellular retention of copper in cancer cells and employs PET imaging with 64Cu to investigate this effect on the whole body level.

scholarly journals Assessment of the role of circulating breast cancer cells in tumor formation and metastatic potential using in vivo flow cytometry

2011 ◽  
Vol 16 (4) ◽  
pp. 040501 ◽  
Author(s):  
Derrick Hwu ◽  
Steven Boutrus ◽  
Cherry Greiner ◽  
Theresa DiMeo ◽  
Charlotte Kuperwasser ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Flow Cytometry ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Metastatic Potential ◽  
Tumor Formation ◽  
In Vivo Flow Cytometry
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