Kuo-Hui su, Ph.D.
Assistant Professor
kuo-hui.su@utoledo.edu
EDUCATION:
| B.S. | 2004 | Physical Therapy | Chung Shan Medical University, Taichung, Taiwan |
| Ph.D. | 2011 | Cardiovascular Physiology | National Yang-Ming University, Taipei, Taiwan |
| Post-Doc | 2012-2014 |
Cardiovascular Physiology |
National Yang-Ming University, Taipei, Taiwan |
| Post-Doc | 2014-2016 | Cell and Cancer Biology | The Jackson Lab, Bar Harbor, ME |
| Post-Doc | 2016-2021 | Cell and Cancer Biology | Mouse Cancer Genetics Program, National Cancer Institute, National Institutes of Health, Frederick, MD |
RESEARCH INTERESTS:
KRAS mutant cancers, such as pancreatic ductal adenocarcinoma (PDAC), which comprises approximately 90% of all pancreatic malignancies, are major contributors to cancer-related deaths. PDAC has a poor prognosis, with a five-year survival rate of less than 6%. In addition, it is typically diagnosed late when metastasis has already occurred, making treatment with surgery or chemotherapy particularly challenging. Heat shock factor 1 (HSF1), a crucial transcriptional factor in proteotoxic stress response (PSR) to maintain proteome homeostasis (proteostasis) via induction of heat shock proteins, plays a pro-oncogenic role in oncogenesis and is highly expressed in several cancer types, including KRAS mutant pancreatic cancer. Apart from HSF1 transcriptional function to maintain protein quality, the transcription-independent role of HSF1 also controls protein quantity and regulates cellular energy metabolism to promote cell growth and tumorigenesis.
Cholesterol accumulation in the pancreas significantly correlates with pancreatic cancer progression. Emerging studies have revealed a link between the PSR and the cellular energy state, such as cholesterol metabolism. High levels of intracellular cholesterol are frequently observed in multiple cancer types and are associated with cancer development, growth, invasion, metastasis, and chemoresistance. In addition, cholesterol trafficking is critical to conserving intracellular cholesterol homeostasis. Furthermore, autophagy has recently been implicated in both the prevention and the progression of cancer. Our research focuses on investigating the role of HSF1 in cholesterol trafficking, lipid metabolic reprogramming, and the autophagy process in pancreatic tumorigenesis via in vitro, in vivo, and preclinical models. The goal of our studies is to reveal novel clinical therapeutic strategies to address these fundamental processes in current cancer therapies.
FUNDING:
Ongoing Research Support
1K22CA248616-01, National Cancer Institute
07/01/2021-06/30/2024
A transcription-independent role of HSF1 in tumorigenesis via suppression of AMPK
Role: PI
University of Toledo, de-Arce-Koch Memorial Endowment Program
5/2/2022-6/30/2023
Role of heat shock factor 1 in pancreatic tumor autophagy
Role: PI
PUBLICATIONS:
STUDENT OPENINGS: Not currently accepting students