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Qun Zhou, MD, PhD

Academic Title:

Associate Professor

Primary Appointment:

Biochemistry and Molecular Biology


Biomedical Research Facility, 337

Phone (Primary):

410-706-1615 (Office)



Education and Training

Dr. Qun Zhou received his PhD  training in Pharmacology and Toxicology from West Virginia University School of Medicine. After completing postdoctoral training in Dr. Nancy Davidson's laboratory at Johns Hopkins University, he started his independent research at the University of Maryland School of Medicine


Highlighted Publications

Yao Y, Li H, Gu Y, Davidson NE, Zhou Q (2010) Inhibition of Class III HDAC Activity Suppresses Estrogen-dependent Gene Transcription. Carcinogenesis 31:382-7 PMID: 19995796

Zhou Q, Chaerkady R, Shaw PG, Kensler TW, Pandey A, Davidson NE (2010) Screening for Therapeutic Targets of Vorinostat by SILAC-based Proteomic Analysis in Human Breast Cancer Cells Proteomics 10:1029-39 PMID: 20049865

Eades G, Yao Y, Yang M, Zhang Y, Chumsri S, Zhou Q (2011) MiR-200a regulates SIRT1 and EMT-like Transformation in Mammary Epithelial Cells. J Biol Chem. 286:25992-6002. PMID:21596753

Li Q, Yao Y, Eades G, Liu Z, Zhang Y, Zhou Q (2013) Downregulation of miR-140 Promotes Cancer Stem Cell Formation in Basal-like Early Stage Breast Cancer. Oncogene. [Epub ahead of print] PMID:23752191

Li Q, Eades G, Yao Y, Zhang Y, Zhou Q (2014) Characterization of a Stem-like Subpopulation in Basal-like Ductal Carcinoma in Situ (DCIS) Lesions. J Biol Chem. 289:1303-122 PMID24297178

Research Interests

Currently, Dr.Zhou's laboratory is focusing on epigenetic regulation of tumor suppressor genes, long non coding RNA, microRNA and cancer stem cells. MicroRNAs (miRNAs) are small non-coding RNAs involved in post-transcriptional gene silencing that are known to regulate differentiation and cell fate and are dysregulated in nearly all human cancers. We have been investigating the roles of miRNAs in normal and transformed breast epithelium, seeking to understand the significance of miRNA dysregulation in breast cancer stem cells.

Our studies have centered to a large extent on microRNAs and yielded considerable insights into molecular mechanisms that suppress transformation potential. We began our work in early stage breast cancer. Ductal Carcinoma In Situ (DCIS), an early stage of human breast cancer, accounts for 20-45% of new cases of breast cancer each year. Patients with DCIS are at high risk for subsequent recurrences and development of invasive breast cancer even after they receive breast-conserving surgery and radiotherapy. Consequently, an important goal of breast cancer prevention is reducing the incidence of DCIS. However, as the molecular mechanisms that underlie DCIS development remain largely unclear, specific pathways that could be targeted for cancer prevention have yet to be identified. Moreover, a lack of information at a mechanistic level often leads to unnecessary treatment (radiotherapy and/or anti-hormone therapy) in cases of benign DCIS that is often associated with adverse toxic effects. For these reasons, our research project seeks to identify the molecular mechanisms that drive DCIS formation. By screening breast cancer tissues and performing array-based miRNA profiling in primary DCIS tissues, we identified that loss of miR-140 expression commonly occurs in DCIS.

Our studies strongly support that miR-140 loss predisposes to DCIS development, which is associated with accumulation of breast cancer stem cells. We have developed novel cell culture-based models and animal models of DCIS, including miR-140 knockout cell lines and knockout mice that are being used in novel ways to gain a complete understating of the mechanisms involved in miR-140 promotion of DCIS. We initiated studies to understand the functional properties of miR-140 important to the development of breast cancer: obtaining a detailed understanding of how epigenetic mechanisms contribute to loss of miR-140 expression, understanding how loss of miR-140 expression alters stem cell self-renewal leading to transformation of normal mammary stem cells into breast cancer stem cells, and understanding how epigenetic therapy restores miR-140 expression and ultimately prevents breast cancer development.