Hani Goodarzi PhD
Hani Goodarzi PhD
Hani Goodarzi, PhD came to UCSF in 2016 from Rockefeller University in New York City where he was a Ruth Kirschstein and Anderson Cancer Center postdoctoral fellow. He completed his PhD dissertation, entitled “Experimental and Computational Approaches for Genetic Dissection of Complex Phenotypes,” at Princeton University in November 2010 in Molecular Biology. During his postdoctoral tenure at the Laboratory of Systems Cancer Biology at Rockefeller University, he discovered several previously uncharacterized post-transcriptional regulatory pathways that drive breast cancer progression and was awarded the Blavatnik Regional Award and The Tri-Institutional Breakout Prize for Junior Investigators.
Our group is a multidisciplinary lab focused on developing integrated computational and experimental strategies in order to uncover the underlying regulatory mechanisms that drive cancer progression and metastasis. For cancer to spread, genes involved in the metastatic process must be altered. This dysregulation largely arises from modulations in the regulatory processes that govern gene expression dynamics. While post-transcriptional regulatory programs are responsible for the fate of RNA molecules in the cell, systematic studies of pathological aberrations in these pathways remain elusive.
A long-standing obstacle in decoding post-transcriptional regulatory programs is accounting for the contribution of local secondary structures in RNA-mediated regulatory interactions. To overcome this challenge, we have developed a computational framework, named TEISER, for discovering structural RNA elements that govern the behavior of RNA in the cell. Having validated this framework and its strength in discovering structural elements with significant contributions to human disease, we seek to identify post-transcriptional regulatory pathways that are co-opted by cancer cells to achieve a higher metastatic capacity.
Using computational, biochemical, and genetic tools, we aim to address the following biological problems: (1) What are the post-transcriptional regulatory programs that govern aberrant splicing patterns in cancer cells? (2) What are the roles of higher-order inter-molecular interactions, including RNA-RNA, RNA-protein, and protein-protein, in shaping the post-transcriptional regulatory networks? (3) What is the contribution of RNA structure to the definition of RNA-mediated interactions and their regulatory consequences? Finding solutions to these problems is a crucial step towards understanding how aberrant activity of post-transcriptional regulatory pathways help initiate and maintain the transformation process. Ultimately, we aim to target these pathological programs, in adjuvant or neoadjuvant settings, to inhibit the progression of metastatic tumors.
University of California San Francisco
Helen Diller Family Cancer Research Building
Department of Urology, MC 3110
1700 4th Street
PO Box 3120
San Francisco, CA 94143