Abstract 1250: Role of mitochondria elongation in p53-induced cellular senescence

Abstract

Abstract Various stresses such as oncogene activation, oxidative stress, and activation of tumor suppressors induce cellular senescence in both normal and cancer cells. This phenomenon, termed premature senescence or accelerated senescence, acts as an important barrier against tumorigenesis and is also considered to be a potential mechanism for controlling human cancers. Although mitochondria has been implicated in cancer, but the exact role of mitochondria in premature senescence has not been fully determined. Here, we studied how morphological and functional change in mitochondria involves in the onset of p53-induced premature senescence. Upon p53 expression in p53-defective cancer cells, extensive elongation of mitochondria network and functional defects in mitochondria were detected. Antioxidant NAC treatment indicates that mitochondria elongation induces increase the level of ROS, which is an important mediator for cellular senescence. Our results suggest that morphology change and subsequent dysfunction of mitochondria play a critical role in p53-induced premature senescence. Citation Format: Young Yeon Kim, Hye Jin Jee, Na Young Jeong, Jeanho Yun. Role of mitochondria elongation in p53-induced cellular senescence. [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 1250. doi:10.1158/1538-7445.AM2015-1250