Assistant Professor
Breast Center
Department of Molecular and Cellular Biology
Baylor College of Medicine
Houston, Texas, United States
Dan L Duncan Comprehensive Cancer Center
Baylor College of Medicine
Houston, Texas, United States
The Therapeutic Innovation Center
Baylor College of Medicine
Houston, Texas, United States


MD from Second Military Medical University
Clinical Anesthesiology
PhD from Second Military Medical University
Biochemistry and Molecular Biology
Postdoctoral Training at Baylor College of Medicine
Cancer multi-OMICS and Targeted Therapy and Resistance

Professional Interests

  • Cancer epitranscriptomics, Multi-OMICS integration, Functional genomics

Professional Statement

Dysregulated cancer epitranscriptomics in targeted therapy resistance

Cancer arises from genetic alterations that invariably lead to dysregulated epigenetic and transcriptional programs. These dysregulated epitranscriptomic events eventually reprogram cancer cells to survive targeted therapies and promote cancer progression and metastasis. Endocrine therapy targeting estrogen receptor (ER), the master transcription factor in ER+ breast cancer, is effective but resistance is common. So far there are few druggable transcription factors, other than ER, are available in clinic. We have recently reported gene amplification and/or overexpression of the forkhead box protein A1 (FOXA1), a pioneer transcription factor for ER-chromatin binding and function, in both preclinical resistance models and clinical specimens of endocrine-resistant metastatic breast cancer. We are currently using integrated multi-OMICS approach and functional genomics to identify novel key downstream effectors of high FOXA1-induced enhancer and transcriptional reprogramming, using our unique panel of resistance models including patient-derived organoids and xenografts. In addition, our research of lineage-specific master transcription factors leads to investigation of new therapeutic strategies to treat other forms of malignancies, including metastatic pancreatic cancer, which shares the similar mechanism of dysregulated epitranscriptomics induced by FOXA1 augmentation.

Discovery of druggable vulnerabilities of therapy-resistant tumors

Recent studies of large-scale screening reveal gene dependency (e.g., by RNAi) and drug sensitivity across a large body of human cancer cell lines. We are currently employing an in silico bioinformatics approach to integrate and analyze data from studies including CCLE (Cancer Cell Line Encyclopedia, Cancer Dependency Map) and GDSC (Genomics of Drug Sensitivity in Cancer). Our primary aim is to nominate genes as new therapeutic vulnerabilities to treat specific forms of cancer with unique genetic background and variant drug responsiveness. Our initial efforts focus on the vulnerabilities of anti-CDK4/6-resistant ER+ breast cancer with promising results undergoing further functional validation.

Selected Publications


Targeting the Mechanism of Hyperactive FOXA1 in Transcriptional Reprogramming Toward Endocrine Resistance and Metastasis in Breast Cancer
- #RP190398 (Co-PI)
Grant funding from CPRIT


Functional genomics
Multi-OMICS integration
Cancer epitranscriptomics
Molecular biology