Email

sjhan@bcm.edu

Positions

Richard E. Buller Professor

Mol & Cell Biology
Baylor College of Medicine
Houston, TX US

Co-Director

Center for Coregulator Research
Baylor College of Medicine
Houston, Texas United States

Faculty Member

Center for Drug Discovery
Baylor College of Medicine

Faculty Member

Therapeutic Innovative Center
Baylor College of Medicine

Faculty Member

Dan L Duncan Comprehensive Cancer Center
Baylor College of Medicine
Houston, Texas United States

Addresses

BCM-Michael DeBakey Center (Office)

Room: BCMM-M804A1
HOUSTON, TX 77030
United States
Phone: (713) 798-6276
sjhan@bcm.edu

Lab (Lab)

BCM-Micheal DeBakey Center
Room: BCMM-M805 and M807
HOUSTON, TX 77030
United States
Phone: (713) 798-6276
sjhan@bcm.edu

Education

Postdoctoral Fellowship at Samsung Biomedical Reserach Institute

03/1997 - Seoul, South Korea

PhD from Seoul National University

02/1997 - Seoul, South Korea

Postdoctoral Fellowship at Baylor College Of Medicine

06/2000 - Houston, Texas United States

MSc from Seoul National University

01/1993 - Gwanak-Gu, Seoul South Korea

Certifications

Medical Degree

Baylor College of Medicine

Honors & Awards

Investigator-Initiated Research Award (2024)

Department of Defense's Office

Mike Hogg Research Award (2016)

Mike Hogg Research Foundation

NURSA (Nuclear Receptor Signaling Atlas) Research Award (2017)

National Institute of Diabetes and Digestive and Kidney Diseases

Cozzarelli Prize Award (2024)

National Academy of Sciences

Richard and Catherin Buller Endowed Professorship (2024)

Baylor College of Medicine

Professional Interests

• Pathogenic Role of Steroid Receptor Coactivator and Nuclear Receptor in Women's Reproductive Disease

Professional Statement

As an estrogen-dependent pro-inflammatory disease, endometriosis is defined as the colonization and growth of endometrial tissues at anatomic sites outside of the uterine cavity, primarily on the pelvic peritoneum and ovaries. Up to 5-10% of reproductive-aged women worldwide suffer chronically from endometriosis symptoms, such as pelvic pain and infertility. Due to the severe chronic morbidity associated with this gynecological disorder, our study has attempted to identify the distinguishing molecular features of endometriotic lesions and endometrial dysfunction to develop more effective prognostic, diagnostic, and treatment strategies for the clinical management of this debilitating disease and the amelioration of endometriosis-associated infertility.

Tregs are essential in restraining immune responses for immune homeostasis. SRC-3 is a pleiotropic coactivator, the second-most highly expressed transcriptional coactivator in Tregs, and a suspect in Treg function. Our study showed that the disruption of SRC-3 expression in Tregs leads to 'complete lifetime eradication' of tumors in aggressive syngeneic breast cancer mouse models because deletion of SRC-3 alters the expression of a wide range of key genes involved in efferent and afferent Treg signaling. SRC-3KO Tregs confer this long-lasting protection against cancer recurrence in mice without an apparent systemic autoimmune pathological phenotype. Therefore, our team will develop the SRC-3 deleted Tregs cell therapy as a novel and efficient future treatment for eliminating tumor growth and recurrence without the autoimmune side-effects that typically accompany immune checkpoint modulators.

Websites

Videos

Selected Publications

• Han SJ, Jung SY , Wu S., Hawkins SM, Park, MJ, Kyo S., Qin J, Lydon JP, Tsai, S.Y., Tsai, M-J., DeMayo FJ, O'Malley BW. "Estrogen Receptor β modulate apoptosis complaex and the inflammasome to drive the pathogensis of endometriosis." Cell. 2015;163(4):960-74. Pubmed PMID: 26544941
• Han SJ, Hawkins SM, Begum K, Jung SY, Kovanci E, Qin J, Lydon JP, Demayo FJ, O'Malley BW "A new isoform of steroid receptor coactivator-1 is crucial for pathogenic progression of endometriosis.." Nat Med. 2012 Jun 3; Pubmed PMID: 22660634
• Park Y, Cho YJ, Sung N, Park MJ, Guan X, Gibbons WE, O'Malley BW, Han SJ. "Oleuropein suppresses endometriosis progression and improves the fertility of mice with endometriosis." J Biomed Sci. 2022 Nov 22;29 Pubmed PMID: 36419064
• Han SJ, Sung N, Wang J, O'Malley BW, Lonard DM. "Steroid receptor coactivator-3 inhibition generates breast cancer antitumor immune microenvironment." Breast Cancer Res.. 2022 Oct 31;24 Pubmed PMID: 36316775

Funding

The Genomic Function of Estrogen Receptor Beta in Endometriosis - #R01 HD098059-01A1

Grant funding from NICHD

The major goals of this project are to define how the specific ER-beta mediated gene network modulate antiapoptosis, epithelial-mesenchymal transition and angiogenesis of endometriotic lesions for the progression of endometriosis.

Development of SRC-3 gene disrupted Tregs for adoptive cell therapy to treat cancer through the modulation of inherent tumor-immune system defenses

Grant funding from CoRegen Inc

The main goal of this project is to develop a new immunotherapy using SRC-3 deleted regulatory T cells to eradicate cancer without adverse effects.

Defining the Critical Module to Cooperatively Control the Estrogen/Growth Factor/Immunity Signaling in Endometriosis Progression - #HT9425-24-1-0254

Grant funding from Department of Defense Office of the Congressionally Directed Medical Research Programs

Endometriosis is a complex disease because aberrant estrogen and growth factor signaling, and immune dysregulation are closely associated for the endometriosis progression. Therefore, what is the key modulator to cooperatively coordinate estrogen/growth factor/immunity axis for the endometriosis progression is the $64 question to understand the nature of the molecular pathogenesis of endometriosis. Unfortunately, this question still needs to be answered. Here, we propose that Hepatocyte Growth Factor activates MET receptor tyrosine kinase (MET) in endometriotic lesions and then directly phosphorylates the Y99 site of Estrogen Receptor beta (ERβ), stimulating its transcriptional activity. The activated MET/ERβ directly elevates the Programmed Death-Ligand 1 (PD-L1) in endometriotic lesions and then generate an endometriotic immune microenvironment to enhance endometriosis progression. Thus, anti-PD-L1 antibody immunotherapy changes the endometriotic immune microenvironment to suppress endometriosis progression and relieve endometriosis-associated symptoms, such as pain and infertility.