In SK-Hep1 cells, AICAR-mediated AMPK activation significantly attenuated resistin-induced adhesion to HUVECs.
In plain wordsIn cells, AICAR reduced resistin-induced cancer cell adhesion to blood vessel cells.
- Peptide
- AICAR (acadesine)
- Outcome
- DecreaseCancer cell adhesion to endothelium
- Study
humann: not reported in source
SK-Hep1 cells and HUVECs- Outcome group
- Tumor growth · Cancer
Source sentences
Moreover, treatment with AICAR demonstrated that AMPK activation in SK-Hep1 cells significantly attenuates the resistin effect on SK-Hep1 cell adhesion to HUVECs.
2 context sentences(design, population, supporting numbers)
Human SK-Hep1 cells were used to study the effect of resistin on intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions as well as NF-κB activation, and hence cell adhesion to human umbilical vein endothelial cells (HUVECs).
5-Aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, was used to determine the regulatory role of AMPK on HCC adhesion to the endothelium in regard to the resistin effects.
In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).