Comparative proteomics as a tool for identifying specific alterations within interferon response pathways in human glioblastoma multiforme cells.

An acquisition of increased sensitivity of cancer cells to viruses is a common outcome of malignant progression that justifies the development of oncolytic viruses as anticancer therapeutics. Studying molecular changes that underlie the sensitivity to viruses would help to identify cases where oncolytic virus therapy would be most effective. We quantified changes in protein abundances in two glioblastoma multiforme (GBM) cell lines that differ in the ability to induce resistance to vesicular stomatitis virus (VSV) infection in response to type I interferon (IFN) treatment.

Prooxidant properties of p66shc are mediated by mitochondria in human cells.

p66shc is a protein product of an mRNA isoform of SHC1 gene that has a pro-oxidant and pro-apoptotic activity and is implicated in the aging process. Mitochondria were suggested as a major source of the p66shc-mediated production of reactive oxygen species (ROS), although the underlying mechanisms are poorly understood. We studied effects of p66shc on oxidative stress induced by hydrogen peroxide or by serum deprivation in human colon carcinoma cell line RKO and in diploid human dermal fibroblasts (HDFs).

[P66shc action on resistance of colon carcinoma RKO cells to oxidative stress].

P66shc protein is an alternative transcript product of SHC1 gene. While two other isoforms (p52shc and p46shc) have adaptor function in RAS signaling pathway, p66shc regulates reactive oxygen species (ROS) level. P66shc genome knockout significantly extends lifespan in mice.