Monitoring circulating cancer cells by multichannel in vivo flow cytometry

2012 ◽  
Author(s):  
Costas Pitsillides ◽  
Konstantinos Kapnisis ◽  
Marianna Prokopi ◽  
Christina Kousparou ◽  
Andreas Anayiotos
Keyword(s):  
Flow Cytometry ◽  
Cancer Cells ◽  
Circulating 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 Studying circulation times of liver cancer cells by in vivo flow cytometry

2011 ◽  
Vol 276 ◽  
pp. 012005
Author(s):  
G Liu ◽  
Y Li ◽  
Z Fan ◽  
J Guo ◽  
X Tan ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Liver Cancer Cells ◽  
In Vivo Flow Cytometry

Circulation times of cancer cells by in vivo flow cytometry

2012 ◽  
Author(s):  
Li Zhang ◽  
Yan Li ◽  
Zhengqin Gu ◽  
Tong Chen ◽  
Cheng Wang ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Cancer Cells ◽  
In Vivo Flow Cytometry

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

scholarly journals Costunolide Induces Apoptosis via the Reactive Oxygen Species and Protein Kinase B Pathway in Oral Cancer Cells

2021 ◽  
Vol 22 (14) ◽  
pp. 7509
Author(s):  
Hai Huang ◽  
Jun-Koo Yi ◽  
Su-Geun Lim ◽  
Sijun Park ◽  
Haibo Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Flow Cytometry ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Migration And Invasion ◽  
Oxygen Species ◽  
Oral Cancer Cells

Oral cancer (OC) has been attracted research attention in recent years as result of its high morbidity and mortality. Costunolide (CTD) possesses potential anticancer and bioactive abilities that have been confirmed in several types of cancers. However, its effects on oral cancer remain unclear. This study investigated the potential anticancer ability and underlying mechanisms of CTD in OC in vivo and in vitro. Cell viability and anchorage-independent colony formation assays were performed to examine the antigrowth effects of CTD on OC cells; assessments for migration and invasion of OC cells were conducted by transwell; Cell cycle and apoptosis were investigated by flow cytometry and verified by immunoblotting. The results revealed that CTD suppressed the proliferation, migration and invasion of oral cancer cells effectively and induced cell cycle arrest and apoptosis; regarding the mechanism, CTD bound to AKT directly by binding assay and repressed AKT activities through kinase assay, which thereby downregulating the downstream of AKT. Furthermore, CTD remarkably promotes the generation of reactive oxygen species by flow cytometry assay, leading to cell apoptosis. Notably, CTD strongly suppresses cell-derived xenograft OC tumor growth in an in vivo mouse model. In conclusion, our results suggested that costunolide might prevent progression of OC and promise to be a novel AKT inhibitor.

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