Abstract #2255

MR compatible cell perfusion system allows investigating metabolism and invasion of hepatocellular carcinoma cells during p53 re-activation induced senescence

Philipp Knopf^1,2, Jesus Pacheco-Torres¹, Flonne Wildes¹, Christoph Trautwein², Benyuan Zhou², Balaji Krishnamachary¹, Lars Zender³, Bernd J. Pichler², and Zaver M. Bhujwalla^1,4,5

¹Division of Cancer Imaging Research, The Russell H Morgan Department of Radiology and Radiological Science, The Johns Hopkins University, School of Medicine, Baltimore, MD, United States, ²Werner Siemens Imaging Center, Department of Preclinical Imaging and Radiopharmacy, Eberhard Karls University Tübingen, Tübingen, Germany, ³Department of Internal Medicine VIII, Eberhard Karls University Tübingen, Tübingen, Germany, ⁴Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University, School of Medicine, Baltimore, MD, United States, ⁵Department of Radiation Oncology and Molecular Radiation Sciences, The Johns Hopkins University, School of Medicine, Baltimore, MD, United States

Here we investigated the metabolic characteristics and the effect of the so called senescence associated secretory phenotype (SASP) on extracellular matrix (ECM) degradation of p53 re-activation induced senescence, using a murine liver carcinoma cell model, where p53 is silenced in the presence of doxycycline hyclate. Senescence is induced within three days after doxycycline hyclate withdrawal and subsequent p53 re-activation. Our data revealed alterations of metabolites in p53-reactivation induced senescent H-Ras cells compared to control cells, including creatine, phosphocreatine and glycerophosphocholine indicating differences in energy and phospholipid metabolism. Senescent H-Ras cells tended to degrade the ECM more than control cells.

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