Our Science – Huang Website

Jing Huang, Ph.D.

Laboratory of Cancer Biology and Genetics Head, Cancer and Stem Cell Epigenetics Section Investigator Center for Cancer Research National Cancer Institute Building 37, Room 3140A Bethesda, MD 20892-4258 Phone:   301-496-2202 Fax:   301-402-1031 E-Mail:   huangj3@mail.nih.gov

Biography

Dr. Huang received his BS in Biochemistry from Peking University. He studied estrogen receptor signaling with Drs. Robert Bambara and Mesut Muyan at the University of Rochester (NY) and received his PhD in 2004. After his postdoctoral training in cancer epigenetics with Dr. Shelley Berger at the Wistar Institute, he joined the Laboratory of Cancer Biology and Genetics as a tenure-track Principal Investigator in October, 2008. Dr. Huang won a NCI Director's Innovation Award with Dr. Jianxin Shi (DCEG) in 2011.

Research

The overarching goal of the Cancer and Stem Cell Epigenetics Section is to develop novel, particularly epigenetic, strategies to combat cancer. We are concentrating on stem cell differentiation, a fascinating epigenetic process. Specifically, we are investigating the roles of p53 signaling in the regulation of stem cell differentiation and how these roles are related to the tumor suppressive function of p53.

We have two complementary projects involving embryonic stem (ES) cells and adult stem cells:

1) We are studying DNA damage stress responses of ES cells, with a focus on p53 signaling. ES cells can develop into almost any cell types and have huge potential in clinical application. However, it is unknown how ES cells maintain their genome stability responding to DNA damage stress. We aim to address this question by studying p53 signaling, one of the major pathways of DNA damage. Our studies as well as others have revealed that p53 plays important roles in the regulation of ES cell differentiation (Li et al., Molecular Cell, 2012; Lee et al., PNAS, 2010).

2) We are also interested in the roles of p53 in the stress responses of adult stem cells. Many tumors have stem cell-like features, self-renewal and multipotency. These tumors could arise from either differentiated cells being reprogrammed into a stem cell-like status or adult stem cells being transformed. Regardless of the cell-of-origin of these tumor cells, p53 is critical to suppress them. The mechanism, however, is largely unclear. We hope to gain insights into the tumor suppressive function of p53 by studying its roles in adult stem cells.

To achieve our goals, we use various techniques, including molecular biology, biochemistry, mouse genetics, genomics (ChIP-seq and RNA-seq) and systems biology.

All the datasets are downloadable from GEO database or click the links on the left of this page.

This page was last updated on 6/7/2013.