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Contact

 

Jing Yang

Affiliation: UCSD SOM
Assistant Professor of Pharmacology and Pediatrics

jingyang@ucsd.edu
Phone: (858) 534-1994

Biography

Jing Yang did her graduate work in the laboratory of Dr. Sally Kornbluth and received her Ph.D. in Molecular Cancer Biology from Duke University, Durham, NC. Her graduate studies focused on dissecting the molecular machinery controlling entry into mitosis during cell cycle progression. She then conducted postdoctoral research on tumor metastasis in the laboratory of Dr. Robert Weinberg at Whitehead Institute, Cambridge, MA. Jing joined the faculty at the University of California, San Diego in 2006.

Research Summary

Although tumor metastasis causes over 90% of cancer deaths, its molecular basis is largely unknown. The research in my laboratory aims to uncover the genes and the signaling pathways responsible for tumor metastasis. Our experimental approaches combine molecular biology tools, mouse tumor models, functional genomics and in vivo imaging techniques.

We have explored a unique mouse breast cancer metastasis model to identify key regulators of tumor metastasis. Our studies discovered that the Twist transcription factor, a master regulator of early embryonic morphogenesis, is essential for the ability of breast tumor cells to metastasize from the mammary gland to the lung. We further demonstrated that Twist contributes to tumor invasion and metastasis by activating a latent developmental program termed an epithelial-mesenchymal transition (EMT). Recently, our and several other studies reported the involvement of Twist and the EMT program in various human malignancies, including breast cancers, gastric cancers, melanomas and neuroblastomas.

Currently, our research focuses on the following areas:
1) The Molecular Machinery: Twist, as a key player in tumor metastasis, may exploit several transcription targets to provoke EMT and other aspects of migration and invasion. We are using genomics, bioinformatics, and biochemical approaches to dissect the signaling and effector pathways that link Twist to EMT and tumor metastasis. We also plan to test the involvement of these signaling pathways in clinical human cancers.
2) The Dynamic Action: The in vivo role of EMT in tumor metastasis is still highly debated. Clinical observations show that the majority of human carcinoma metastases present an epithelial morphology in distant organs. We propose that carcinoma cells undergo EMT to invade and disseminate. Once reaching distant organs, these mesenchymal cells will reverse to an epithelial identity in order to regain proliferating ability. We have established mouse tumor models to determine how Twist and EMT contribute to tumor metastasis in vivo.
3) The Inducing Signals: The ability of carcinoma cells to undergo EMT and metastasize depends on both their genetic/epigenetic alternations and the environmental cues they receive. Several signaling pathways, including TGF-beta, Wnt, and Notch, are involved in activating cell migration and tissue rearrangement during normal development. We are very interested in exploring the roles of such signals in inducing Twist, EMT and tumor metastasis.
4) The Novel Players: Our previous study identified a number of new candidate genes involved in tumor metastasis. We will explore their biological functions in tumor metastasis using cell culture models, mouse tumor models, and clinical human tumor samples.

References

References From PubMed (NCBI)

 

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©2008 UCSD/Burnham Molecular Pathology Graduate Program