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Jing Huang, Ph.D.

Portait Photo of Jing Huang
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 the estrogen receptor signaling in breast cancer 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's section is currently study the roles of p53 in stem cells. 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 strategies to combat cancer. We concentrate on studying 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 functions 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 many different 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. We and others have found 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 contain cells that have stem cell-like features, self-renewal and multipotency. These stem-like cells 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 for suppressing the stem-like phenotype. The mechanism, however, is largely unclear. We are currently studying the roles of p53 in adult stem cells with the hope to gain insights into the lineage control and the tumor suppressive function of p53.

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 the GEO database or through the links on the left of this page.

This page was last updated on 11/25/2013.