scholarly journals Hypoxia induces CXCR4 expression and biological activity in gastric cancer cells through activation of hypoxia-inducible factor-1α

2012 ◽  
Vol 28 (6) ◽  
pp. 2239-2246 ◽  
Author(s):  
YOON SUK OH ◽  
HA YON KIM ◽  
IK-CHAN SONG ◽  
HWAN-JUNG YUN ◽  
DEOG-YEON JO ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Biological Activity ◽  
Cancer Cells ◽  
Hypoxia Inducible Factor ◽  
Cxcr4 Expression ◽  
Gastric Cancer Cells ◽  
Hypoxia Inducible Factor 1Α

scholarly journals Hypoxia regulates CD44 expression via hypoxia-inducible factor-1α in human gastric cancer cells

2016 ◽  
Vol 13 (2) ◽  
pp. 967-972 ◽  
Author(s):  
Gai Liang ◽  
Shuang Li ◽  
Wei Du ◽  
Qinghua Ke ◽  
Jun Cai ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Hypoxia Inducible Factor ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Cd44 Expression ◽  
Hypoxia Inducible Factor 1Α

Chemokine receptor CXCR4 expression and its regulation in gastric cancer cells

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e22173-e22173
Author(s):  
H. Lee ◽  
H. Kim ◽  
S. Kim ◽  
H. Yun ◽  
S. Kim ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Flow Cytometry ◽  
Steady State ◽  
Cancer Cells ◽  
Chemokine Receptor ◽  
Cxcr4 Expression ◽  
Human Gastric Cancer ◽  
Rt Pcr ◽  
Gastric Cancer Cells ◽  
Membrane Expression

e22173 Background: The chemokine receptor CXCR4 is associated with the biological behavior in several kinds of cancer, but few studies have addressed the expression and regulation of CXCR4 in gastric cancer. Methods: Five gastric cancer cell lines were studied. The expression of CXCR4 was investigated using RT-PCR, Westerning blotting, flow cytometry, and immunofluorescence staining. The regulation of CXCR4 expression by hypoxia, dexamethasone, and the proinflammatory cytokines was evaluated. Results: CXCR4 mRNA and proteins were detectable by RT-PCR and Western blot analysis, respectively, in all five cell lines. However, MKN-28, MKN-45, MKN-74, and SNU 16 cells did not express membrane CXCR4, but had abundant CXCR4 in their cytoplasm, as determined by flow cytometry and immunofluorescence staining. In contrast, a small population of KATO III cells expressed membrane CXCR4. Hypoxia up-regulated CXCR4 proteins and enhanced membrane expression of CXCR4 in human gastric cancer KATO III cells, which constitutively expressed membrane CXCR4 in a steady state, as revealed by Western blotting and flow cytometry, respectively. This hypoxia-induced expression of CXCR4 was mediated via hypoxia-inducible factor (HIF)-1α. In addition, KATO III cells exposed to hypoxia demonstrated enhanced migration in response to stromal cell-derived factor (SDF)-1α, a specific ligand for CXCR4. However, MKN-28, MKN-45, MKN-74, and SNU-16 cells, which lack membrane CXCR4 in a steady state, showed no change in CXCR4 expression in hypoxic condition. Treatment with IFN-γ, TGF-β, TNF-α, and dexamethasone did not induce any change in CXCR4 expression in all five gastric cancer cells. Conclusions: This study suggests that hypoxia up-regulates the membrane expression of functional CXCR4 via HIF-1α in human gastric cancer cells that basally express membrane CXCR4 in a steady state in vitro. No significant financial relationships to disclose.

Sign in / Sign up

Export Citation Format

Share Document