Human cancer cells are subjected to hypoxic conditions in many tumours. Hypoxia causes alterations in the glycolytic pathway activation through stabilization of hypoxia-inducible factor 1. Currently, two approaches are commonly used to model hypoxia: an alternative to generating low-oxygen conditions in an incubator, cells can be treated with CoCl 2.
We performed RNA-seq experiments to study transcriptomes of human Caki-1 cells under real hypoxia and after CoCl 2 treatment. Despite causing transcriptional changes of a much higher order of magnitude for the genes in the hypoxia regulation pathway, CoCl 2 treatment fails to induce alterations in the glycolysis / gluconeogenesis pathway. Moreover, CoCl 2 caused aberrant activation of other oxidoreductases in glycine, serine and threonine metabolism pathways.
F1000Research. 2015 Dec 30*** epublish ***
Nadezhda Zhigalova, Artem Artemov, Alexander Mazur, Egor Prokhortchouk
Institute of Bioengineering, Research Center of Biotechnology RAS, Moscow, Russian Federation., Institute of Bioengineering, Research Center of Biotechnology RAS, Moscow, Russian Federation., Institute of Bioengineering, Research Center of Biotechnology RAS, Moscow, Russian Federation., Institute of Bioengineering, Research Center of Biotechnology RAS, Moscow, Russian Federation.