Regulation of signalling pathways by extracellular calcium in colon cancer cells

Bone ◽  
2012 ◽  
Vol 51 (6) ◽  
pp. S22
Author(s):  
S. Tennakoon ◽  
B. Marian ◽  
J. Schmid ◽  
E. Kállay
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Extracellular Calcium ◽  
Signalling Pathways ◽  
Colon Cancer Cells

Docosahexaenoic acid sensitizes colon cancer cells to apoptotic effect of TRAIL by modulation of lipid and apoptotic signalling pathways

2011 ◽  
Vol 164 ◽  
pp. S33
Author(s):  
Belma Skender ◽  
Alena Vaculová ◽  
Josef Slavík ◽  
Miroslav Machala ◽  
Alois Kozubík ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Docosahexaenoic Acid ◽  
Cancer Cells ◽  
Signalling Pathways ◽  
Colon Cancer Cells ◽  
Apoptotic Effect

scholarly journals Stereo-Specific Modulation of the Extracellular Calcium-Sensing Receptor in Colon Cancer Cells

2021 ◽  
Vol 22 (18) ◽  
pp. 10124
Author(s):  
Martin Schepelmann ◽  
Nadja Kupper ◽  
Marta Sladczyk ◽  
Bethan Mansfield ◽  
Teresa Manhardt ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Inflammatory Cytokine ◽  
Extracellular Calcium ◽  
Colon Cancer Cells ◽  
Calcium Sensing Receptor ◽  
Hek 293 ◽  
Calcium Sensing ◽  
293 Cells ◽  
Target Effects

Pharmacological allosteric agonists (calcimimetics) of the extracellular calcium-sensing receptor (CaSR) have substantial gastro-intestinal side effects and induce the expression of inflammatory markers in colon cancer cells. Here, we compared the effects of both CaSR-specific (R enantiomers) and -unspecific (S enantiomers) enantiomers of a calcimimetic (NPS 568) and a calcilytic (allosteric CaSR antagonists; NPS 2143) to prove that these effects are indeed mediated via the CaSR, rather than via off-target effects, e.g., on β-adrenoceptors or calcium channels, of these drugs. The unspecific S enantiomer of NPS 2143 and NPS S-2143 was prepared using synthetic chemistry and characterized using crystallography. NPS S-2143 was then tested in HEK-293 cells stably transfected with the human CaSR (HEK-CaSR), where it did not inhibit CaSR-mediated intracellular Ca2+ signals, as expected. HT29 colon cancer cells transfected with the CaSR were treated with both enantiomers of NPS 568 and NPS 2143 alone or in combination, and the expression of CaSR and the pro-inflammatory cytokine interleukin 8 (IL-8) was measured by RT-qPCR and ELISA. Only the CaSR-selective enantiomers of the calcimimetic NPS 568 and NPS 2143 were able to modulate CaSR and IL-8 expression. We proved that pro-inflammatory effects in colon cancer cells are indeed mediated through CaSR activation. The non-CaSR selective enantiomer NPS S-2143 will be a valuable tool for investigations in CaSR-mediated processes.

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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