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CB-13PHENOTYPIC CHANGES BY NUCLEAR-ENCODED CYTOCHROME C OXIDASE SUB-UNIT 4, ISOFORM 1 SUPPORTS POOR PROGNOSTIC IN GBM PATIENTS
Abstract   Open access   Peer reviewed

CB-13PHENOTYPIC CHANGES BY NUCLEAR-ENCODED CYTOCHROME C OXIDASE SUB-UNIT 4, ISOFORM 1 SUPPORTS POOR PROGNOSTIC IN GBM PATIENTS

Claudia Oliva, Nathaniel Reeve, Tara Markert and Corinne E. Griguer
Neuro-oncology (Charlottesville, Va.), Vol.16(Suppl 5), pp.v43-v43
11/01/2014
DOI: 10.1093/neuonc/nou241.12
PMCID: PMC4217949
url
https://doi.org/10.1093/neuonc/nou241.12View
Published (Version of record) Open Access

Abstract

Cytochrome c Oxidase is a mitochondrial enzyme involved in cellular respiration and production of energy. Previously, we demonstrates that a high enzymaticl activity is associated with poor overall survival in GBM patients () and chemoresistance to Temozolomide. Thus, we hypothesize that CcO may be directly involved in the aggressive phenotype of these tumors. Elevated CcO activity is associated with a switch in CcO subunit 4. We use gene targeting of CcO sub-unit 4 isoform 1 or 2 (COX4i1 and COX4i2) and patient xenoline tumors. Genetic swap between COX4i2 and COX4i1 significantly increased tumor growth and proliferation in vitro and in vivo. However, under hypoxic condition, COX4i1 cells stopped proliferating and became more invasive. Our results support the view that COX subunit 4-1 drives tumor cell growth, proliferation and invasion. Moreover, manipulation of COX4 isoforms uncoupled cell proliferation from cell invasion; this control is hypoxia –dependent. This result provides evidence for a novel role for CcO beside its mitochondrial function. Supported by P20 CA151129-02 (NCI SPORE Program) and R01 CA160821 (USPHS/NIH/NCI)
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