Abstract 3054: Bioenergetic Signature of Stromal Cells Defines the Aggressiveness of Prostate Cancer

Abstract Cancer-associated fibroblasts, though derived from multiple lineages, share common as well as unique characteristics and play a critical role in various aspects of neoplasia. Their activities range from contributing to tumor formation to promoting the growth and invasion of tumors. They also promote angiogenesis, provide a metabolically friendly tumor environment, and confer resistance to chemotherapy and radiation. Clinical trials targeting stromal cells were disappointing. The reason underlying this failure has been ascribed to the fact that stromal cells do change during cancer progression to aggressive form. As the cancer progresses, both prostate cancer cells as well as stromal cells have to ‘functionally adapt’ to the microenvironment within the tumor mass and mutually support their growth in a hostile environment. The major environmental factor that molds the biology of cancer cells and stromal components is low oxygen tension within the tumor. The key cellular organelle that is functionally affected by exposure to different oxygen tensions is the mitochondria. In this study we present the data on the progressive changes in the stromal cell mitochondrial function in relation to the aggressiveness of prostate cancer at atmospheric oxygen and at different oxygen tensions. This study reveals the potential use of mitochondrial functional assay for the screening of compounds that specifically target the bioenergetics of stromal cells. This information may also unravel the metabolic interaction between tumor- microenvironment that contributes to tumor development and progression of prostate cancer and potential mechanism of resistance to therapy offered by stromal cells. Citation Format: Praveen Kumar Vayalil, Aimee Landar. Bioenergetic signature of stromal cells defines the aggressiveness of prostate cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3054. doi:10.1158/1538-7445.AM2015-3054