Mitochondrial DNA mutation stimulates prostate cancer growth in bone stromal environment.

Publication Type:

Journal Article

Source:

The Prostate, Volume 69, Issue 1, p.1-11 (2009)

Keywords:

2009, Animals, Bone and Bones, Bone Neoplasms, Cell Division, Cell Line, Tumor, Cell Movement, Cell Survival, Center-Authored Paper, Disease Models, Animal, DNA, Mitochondrial, Fibroblast Growth Factor 1, Focal Adhesion Protein-Tyrosine Kinases, Gene Expression Regulation, Neoplastic, Genomics Core Facility, Human Biology Division, Humans, Male, MICE, Mice, Nude, Mutation, Neoplasm Transplantation, Oligonucleotide Array Sequence Analysis, Prostatic Neoplasms, Shared Resources, Stromal Cells, Transplantation, Heterologous

Abstract:

Mitochondrial DNA (mtDNA) mutations, inherited and somatically acquired, are common in clinical prostate cancer. We have developed model systems designed to study specific mtDNA mutations in controlled experiments. Because prostate cancer frequently metastasizes to bone we tested the hypothesis that mtDNA mutations enhance prostate cancer growth and survival in the bone microenvironment.