Positions

Assistant Professor
Molecular & Cellular Biology
Baylor College of Medicine
Houston, Texas, United States
Faculty Senator
Baylor College of Medicine
Houston, Texas, United States
Member
Dan L Duncan Comprehensive Cancer Center
Baylor College of Medicine
Houston, Texas, United States

Education

BSc from Jilin University
PhD from Institute of Biophysics, Chinese Academy of Sciences
Postdoctoral Training at Baylor College of Medicine

Honors & Awards

Breakthrough Award Funding Level 2
Principle Investigator
Collaborative Research Project with AHMMRF
Principle Investigator
Idea Development Award
Principle Investigator
Individual Investigator Research Award
Principle Investigator
Idea Development Award
Principle Investigator
New Investigator Award
Principle Investigator
Concept Award
Principle Investigator
Exploration-Hypothesis Development Award
Principle Investigator

Professional Interests

  • MAPK4 biology in human cancers
  • Signaling Pathways Regulating Prostate Cancer
  • Therapy-resistance of Human Cancers
  • Mouse Models for Human Cancers
  • Tumor Microenvironment

Professional Statement

Focusing on cancer research, educating researchers, making discoveries, and turning discoveries into effective therapies for cancer patients.

Selected Publications

Projects

MAPK4 biology in human cancers
MAPK4 is an atypical MAPK that were not well studied. MAPK4 biology in human diseases, including cancers, remain largely unknown. We discovered that MAPK4 activates the Akt/mTOR signaling pathway along with several other key pathways to promote cancer initiation, progression, and the development of therapy-resistance. We are now pioneering the research on MAPK4 biology in human cancers and are carrying out in-depth studies to reveal the molecular mechanisms underlying MAPK4 regulation of human cancers.
Targeting GATA2 degradation as a novel therapeutic approach for therapy-resistant prostate cancer
Androgen deprivation therapy (ADT) is the standard therapy for advanced/metastatic prostate cancer (PCa). However, patients inevitably develop the lethal castration-resistant PCa (CRPC) including those resistant to the most advanced therapies using enzalutamide, apalutamide, and abiraterone. Taxane chemotherapy is the first-line treatment for CRPC; however, resistance rapidly occurs. Most CRPCs and taxane-resistant CRPCs remain AR-dependent while the AR- CRPCs are increasingly being observed. GATA2 is a transcription factor and pioneer factor crucial for inducing AR expression and activation in PCa. It can also promote PCa resistance to taxane chemotherapy independent of AR. Therefore, GATA2 is emerging as a therapeutic target for the lethal CRPC/taxane-resistant CRPC. Although it is challenging to directly inhibit GATA2 transcriptional activity, GATA2 protein is unstable, which makes further enhancing GATA2 protein degradation a promising therapeutic avenue. However, how GATA2 protein stability is regulated in PCa remains largely unknown. Over the last five years, we have characterized the detailed molecular mechanism regulating GATA2 stability in PCa. We are now investigating targeting GATA2 degradation as a novel therapeutic approach for prostate cancer, especially the lethal CRPC and taxane-resistant CRPC.
A versatile model for tumor-specific gene manipulation in vivo.
We have developed a versatile gene delivery system for efficient and tumor specific gene manipulation in vivo. This include the RCI-Oncogene/TuKO (tumor specific knockout of gene of interest) system that we have used in revealing a crucial role of FGFR1 in promoting breast cancer progression and most importantly, metastasis.
Ai-Myc model for Cre-induced tissue-specific expression of c-Myc in vivo
c-Myc is the most significantly amplified oncogene in human prostate cancer. Dr. Sawyer’s group has developed the Hi-MYC model using an enhanced probasin promoter to drive c-Myc expression in prostate epithelia. These mice developed invasive prostate carcinomas that shared molecular features with human prostate cancers. This study, along with others, provided crucial data supporting key roles of c-Myc oncogenic pathway in prostate tumorigenesis. However, since probasin promoter activity is crucially dependent on androgen, the prostate tumors lose c-Myc oncogene expression upon castration in such MYC models. Therefore, the tumor regression in these androgen-depleted MYC mice represents the mixed effects of both artificial direct effects from loss of oncogene expression and potential real effects from tumor cellular responses to castration. These greatly limit the abilities to use such models to concisely study androgen signaling, castration-responses, and castration-resistance of prostate cancer. Accordingly, we have developed a novel transgenic model that allows maintained expression of c-Myc oncogene along with luciferase (for real-time in vivo bioluminescence imaging) in prostate after castration. We are performing detailed characterization of this model and using it to study therapy-resistance such as castration-resistance and chemoresistance of prostate cancers.
Tumor microenvironment regulation of prostate cancer
Tumor microenvironment, including stromal cells, has been documented to play key roles in regulating human cancers. Our study revealed that prostate stromal cells profoundly regulate prostate cancer biology, including inducing androgen-dependent and androgen-independent AR activation. We are now investigating the detailed molecular mechanisms underlying this tumor stroma-induced AR activation in prostate cancer cells in the absence of significant amount of androgen. This may provide a direct mechanism for relapse of the lethal castration-resistant prostate cancer after androgen-deprivation therapy.
FGFR1 signaling in prostate cancer and breast cancer.
We are investigating the biological functions of FGFR1 in prostate cancer and breast cancer, focusing on its role in promoting tumor progression and metastasis.