Differential expression of nanog1 and nanogp8 in colon cancer cells

2012 ◽  
Vol 418 (2) ◽  
pp. 199-204 ◽  
Author(s):  
Tatsuya Ishiguro ◽  
Ai Sato ◽  
Hirokazu Ohata ◽  
Hiroaki Sakai ◽  
Hitoshi Nakagama ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Differential Expression ◽  
Colon Cancer Cells

Inhibitory effect of glucocorticoid receptor on colorectal cancer growth by inhibiting glycolysis through autophagy

2020 ◽  
Vol 10 (3) ◽  
pp. 363-373
Author(s):  
Zhiheng Xu ◽  
Kailun Yang ◽  
Xiaohua Li
Keyword(s):  
Colon Cancer ◽  
Lactic Acid ◽  
Glucocorticoid Receptor ◽  
Cell Viability ◽  
Cancer Cells ◽  
Differential Expression ◽  
Malignant Tumors ◽  
Colon Cancer Cells ◽  
Acid Accumulation ◽  
And Migration

Glucocorticoid receptor (GR) affects the development and progression of most malignant tumors by regulating autophagy. The GR gene is not expressed in colon cancer. To explore the role and mechanism of GR in colon cancer, dexamethasone (DXM) was used to stimulate the expression of GR. The expression of the autophagy markers Beclin 1 (BECN1) and light chain 3 (LC3B) was then detected by qRT-PCR and western blotting. The effects of the differential expression of GR on autophagy, ATP, lactic acid accumulation, and glucose utilization in colon cancer cells were studied. Differential expression of GR affected glycolysis, apoptosis, and migration of colon cancer cells, as determined by flow cytometry and cell viability and migration assays, respectively. The DXM-induced elevation of GR expression significantly promoted the expression of the autophagy-related genes BECN1 and LC3B, and decreased the ATP production, lactic acid accumulation, and glucose uptake in colon cancer cells. These events resulted in the inhibition of colon cancer cell growth, which also involved decreased cell viability and mobility and increased rate of apoptosis. These findings indicate that the GR can promote autophagy and inhibit glycolysis in colon cancer cells, reduce their proliferation and migration, and promote their apoptosis in vitro.

Leptin is a growth factor for human colon cancer cells

2001 ◽  
Vol 120 (5) ◽  
pp. A493-A493
Author(s):  
J HARDWICK ◽  
G VANDENBRINK ◽  
S VANDEVENTER ◽  
M PEPPELENBOSCH
Keyword(s):  
Colon Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells

Silencing of a death associated protein kinase as a pro-survival factor in colon cancer cells

Endoscopy ◽  
2005 ◽  
Vol 37 (05) ◽  
Author(s):  
GA Doherty ◽  
SM Byrne ◽  
SC Austin ◽  
GM Scully ◽  
EW Kay ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Survival Factor ◽  
Death Associated Protein Kinase

Cytotoxic Effect of the Combination of Gemcitabine and Atorvastatin Loaded in Microemulsion on the HCT116 Colon Cancer Cells

2017 ◽  
Vol 9 (2) ◽  
Author(s):  
Mayson H. Alkhatib ◽  
Dalal Al-Saedi ◽  
Wadiah S. Backer
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Therapeutic Potential ◽  
Morphological Changes ◽  
In Vitro Study ◽  
Colon Cancer Cells ◽  
Apoptosis Detection ◽  
Hct116 Cells

The combination of anticancer drugs in nanoparticles has great potential as a promising strategy to maximize efficacies by eradicating resistant, reduce the dosage of the drug and minimize toxicities on the normal cells. Gemcitabine (GEM), a nucleoside analogue, and atorvastatin (ATV), a cholesterol lowering agent, have shown anticancer effect with some limitations. The objective of this in vitro study was to evaluate the antitumor activity of the combination therapy of GEM and ATVencapsulated in a microemulsion (ME) formulation in the HCT116 colon cancer cells. The cytotoxicity and efficacy of the formulation were assessed by the 3- (4,5dimethylthiazole-2-yl)-2,5-diphyneltetrazolium bromide (MTT) assay. The mechanism of cell death was examined by observing the morphological changes of treated cells under light microscope, identifying apoptosis by using the ApopNexin apoptosis detection kit, and viewing the morphological changes in the chromatin structure stained with 4′,6-diamidino-2-phenylindole (DAPI) under the inverted fluorescence microscope. It has been found that reducing the concentration of GEM loaded on ME (GEM-ME) from 5μM to 1.67μM by combining it with 3.33μM of ATV in a ME formulation (GEM/2ATV-ME) has preserved the strong cytotoxicity of GEM-ME against HCT116 cells. The current study proved that formulating GEM with ATV in ME has improved the therapeutic potential of GEM and ATV as anticancer drugs.

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