Name：Xin-Hai Pei

Position：Professor

E-mail：peixinhai@szu.edu.cn

Personal Statement:

Dr. Pei got his Ph.D. from Kyushu University in 2000. He has a broad background in both clinical and basic research.  As a clinician, he devoted himself to clinical cancer research for 11 years before switching to basic cancer research. As a postdoctoral fellow and assistant professor at UNC-CH, he generated 5 strains of knockout mice and characterized more than 30 different mouse mutants. He discovered that p18 is a downstream target of GATA3 and restrains mammary luminal tumorigenesis (Pei, Cancer Cell, 2009). As a tenure track assistant and associate professor at the University of Miami, Dr. Pei published 17 research papers. he found that CUL9 ubiquitin ligase is a tumor suppressor, and CUL9 mediates the functions of the 3M complex and ubiquitylates survivin to maintain genome integrity (Pei, Cancer Res. 2011; and Li, Molecular Cell, 2014). He discovered that deletion of Brca1 causes luminal-to-basal mammary tumor transformation, and activates EMT promoting tumor metastasis (Bai, Oncogene, 2013; Cancer Res., 2014). His research was supported by 13 grants ($2.7 million) from federal, state, and private agencies. He earned 2010 and 2013 CDMRP-Breast Cancer Research Program awards, and 2017 Florida Department of Health-Bankhead Coley Cancer Research Grant Award.

Since Oct 2018, he has been moving to China and working as a professor at the Shenzhen University. He, as a director of Shenzhen University Animal Center, has also been in charge of building up and managing the animal center. In addition to the abovementioned research areas, he is also interested in 1) how DNA damage regulates cell fate; 2) how cell cycle inhibitors and transcription factors control cochlea hair cells in hearing loss. He discovered that GATA3 functions downstream of BRCA1 to suppress EMT in cancers (Bai, Theranostics, 2021; 2022; Bai, Cell Death and Disease, 2022; Liu, Cell Death and Disease, 2023; Wang, BMC Biology, 2024), PAPAS promotes differentiation suppressing tumorigenesis (Ren, Cell Reports, 2024), and BRCA1 prevents DNA damage-induced hearing loss (Journal of Neuroscience, 2024).

Research Interests:

DNA damage and diseases

Cell cycle control and tumorigenesis

Genetics and animal model

Research Projects:

1. NSFC (China) Project (82372635):  01/01/2024 to 12/31/2027.  ￥490,000.

2. NSFC (China) Project (81972637):  01/01/2020 to 12/31/2023.  ￥510,000.

3. Guangdong Basic and Applied Basic Research Foundation (2024A1515013103):  01/01/2024 to 12/31/2026.  ￥150,000.

4. Florida Department of Health- Cancer Research Award ( 7BC07):  3/1/17 to 2/28/18.  $97,880.

5. CDMRP-Breast Cancer Research Program- Idea Expansion Award (W81XWH1310282):  9/1/2013 to 8/31/2016.  $537,779.

6. CDMRP-Breast Cancer Research Program-Idea Award (W81XWH-10-1-0302):  4/15/2010 to 5/14/2012.  $554,491

Selected Peer-reviewed Publications:

1. Jiang W^#, Wang G^#, Bai F, Hu B, Xu Y, Xu X, Nie G, Zhu WG, Chen F, and Pei XH*. BRCA1 promotes repair of DNA damage in cochlear hair cells and prevents hearing loss. The Journal of Neuroscience.2024, Oct 16;44(42):e0132242024..

2. Liu X, Bai F*, Wang Y, Wang C, Chan HL, Zheng C, Fang J, Zhu WG, and Pei XH*. Loss of function of GATA3 regulates FRA1 and c-FOS to activate EMT and promote mammary tumorigenesis and metastasis. Cell Death & Disease. 2023, Jun 23;14(6):370..

3. Bai F, Zhang L, Liu X, Wang C, Zheng C, Sun J, Li M, Zhu WG, Pei XH*. GATA3 functions downstream of BRCA1 to suppress EMT in breast cancer. Theranostics. 2021, Jul 13, 11(17):8218-8233..

4. Bai F^#, Chan HL^#, Scott A, Smith MD, Fan C, Herschkowitz JI, Perou, CM, Livingstone AS, Robbins DJ, Capobianco AJ, Pei XH*.  BRCA1 suppresses epithelial-to-mesenchymal transition and stem cell dedifferentiation during mammary and tumor development. Cancer Research. 2014;74(21):6161-6172..

5. Pei XH^#, Bai F^#, Smith MD, Usary J, Fan C, Pai SY, Ho IC, Perou CM, Xiong Y*. CDK inhibitor p18^INK4c is a downstream target of GATA3 and controls mammary luminal progenitor cell proliferation and tumorigenesis. Cancer Cell. 2009;15: 389-401.