PubMed 12586336

Referenced in: none

Automatically associated channels: Kv1.1 , Kv1.2 , Kv1.3 , Kv1.4 , Kv1.5 , Kv1.6 , Kv2.1 , Kv3.1 , Kv3.3 , Kv3.4 , Kv4.2 , Kv9.3

Title: Impaired voltage-gated K+ channel expression in brain during experimental cancer cachexia.

Authors: Mireia Coma, Rubén Vicente, Sílvia Busquets, Neus Carbó, Michael M Tamkun, Francisco J López-Soriano, Josep M Argilés, Antonio Felipe

Journal, date & volume: FEBS Lett., 2003 Feb 11 , 536, 45-50

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/12586336

Abstract
Cancer-induced cachexia affects most advanced cancer patients. It is characterized by anorexia, profound metabolic dysfunctions, and severe neurological disorders. Here we show that voltage-gated potassium channel (Kv) expression is impaired in the brain of tumor-bearing animals. Expression of both delayed rectifier (Kv1.1, Kv1.2, Kv1.3, Kv1.5, Kv1.6, Kv2.1, Kv3.1, Kv4.2) and A-type potassium channels (Kv1.4, Kv3.3, Kv3.4) was greatly down-regulated in brain from animals bearing a Yoshida AH-130 ascites hepatoma. The possible compensatory mechanisms (Kv1.4/Kv4.2), expression of redundant genes (Kv3.1/Kv3.3) and heteromultimeric channel formation (Kv2.1/Kv9.3) were also affected. The high circulating levels of TNFalpha and the reduced expression of the anti-apoptotic protein Bcl-XL found in the brain of tumor-bearing animals indicate that this response could be mediated by an increase in brain cell death due to apoptosis. The results suggest that brain function is impaired during cancer cachexia, and may account for the cancer-induced anorectic response and other neurological alterations.