Pengcheng Bu

Biography

2004-2007 Institute of Biophysics, Chinese Academy of Sciences, Ph.D. 2008-2010 UC Berkeley, Postdoctoral fellow 2010-2015 Cornell University, Research Associate 2015-2016 Duke University, Senior Research Scientist 2016.09-present Institute of Biophysics, Chinese Academy of Sciences, Professor 2004-2007 Institute of Biophysics, Chinese Academy of Sciences, Ph.D. 2008-2010 UC Berkeley, Postdoctoral fellow 2010-2015 Cornell University, Research Associate 2015-2016 Duke University, Senior Research Scientist 2016.09-present Institute of Biophysics, Chinese Academy of Sciences, Professor

Research Interest

Non-coding RNAs (ncRNAs) such as microRNAs and long non-coding RNAs (lncRNAs) occupy the bulk of the genome, but their functions are often obscure. Global dysregulation of microRNAs and lncRNAs in cancers have been consistently reported, though ncRNA deletions often generate no phenotypes in normal tissue homeostasis. Why does the genome devote the bulk of its content to such “dark matter” that performs no function under normal physiology, and why do they become more important in cancer? What are the ncRNA associated proteins? Can we treat cancers by targeting ncRNA associated proteins? Stem cells and differentiated cells have distinct behaviors. Growing evidences showed that changes in energy balance and metabolic status are critical for stem cells. However, many questions are still unclear. For example, how does metabolism regulate intestine/colon homeostasis and regeneration? How does metabolism impact colon cancer initiation and metabolism? Does dietary change benefit colon cancer prevention and therapy? Growing from a single stem cell, intestine/colon organoid can form mini-gut structure, containing stem cells and all the progenies, which makes it a useful model for basic research and clinical applications, especially for biomarker identification and drug screening. Our research is attempting to identify novel biomarkers, especially druggable ncRNAs and metabolic enzymes targeting colon cancer initiation and metastasis. We are developing organoids and mouse models for drug screening and mechanism study.