分子生物标志物与诊断杂志

In-vitro "Depletion" of Mitochondrial Cytochrome C Oxidase Subunit II Affects the Patterns of Gene Expression across Multiple Cancer Pathways

Abstract

Mai A Masri, Nuha M. Elhassan, Hiba S. Mohamed, Christina Wasunna, Abukashawa S and Muntaser E. Ibrahim

There is mounting molecular evidence to suggest mitochondrial malfunctions as a key element in turning-on the vicious circle of oncogenesis in the human body. Cytochrome c oxidase II (MT-CO2) encoded by mitochondrial DNA, and implicated in a number of tumors, has been shown to bind directly to cytochrome c and is speculated to regulate apoptosis through this affinity for cytochrome c. In an attempt to understand the effect of MT-CO2 depletion on the cell function we employ RNA interference and low density arrays encompassing six cancer pathways to gain insights on the potential effect on gene expression caused by siRNA specific to MT-CO2. The results show that MTCO2 knock- down initiated differential expression in eleven genes involved in different pathways including cell cycle, signaling, apoptosis and Angiogenesis, indicating that mtDNA and sMT-CO2 in particular may be key players in the stability of the genome and its functions during tumoregensis.