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Yun Qiu, PhD

Academic Title:


Primary Appointment:


Secondary Appointment(s):



HSF-1, 522C

Phone (Primary):

(410) 706-4535

Education and Training

  • Ph.D., Rutgers University, 1995
  • Postdoctoral Fellow, Case Western Reserve University School of Medicine, 1995-1997


My Ph.D training was done under supervision of Dr. Robert M. Krug at Rutgers University. I studied the functions of influenza virus NS1 protein as an RNA binding protein to regulate host mRNA  nuclear export and splicing. After completing Ph.D degree in 1995, I joined Dr. Hsing-Jien Kung's lab at Case Western Reserve Univrsity School of Medicine as a postdoc fellow, focusing on the mechanisms of signal transduction by protein kinases and how they diversify their signaling in cancer cells. In 1998, I joined University of Minnesota School of Medicine as a tenure track Assitant Professor in Deprtment of Lab Medicine & Pathology, where my lab continued to study the role of several tyrosine kinases in prostate cancer cells. In 2002, my lab moved to University of Maryland School and Medicine. The current research interests in my lab are focused on molecular mechnisms underlying therapeutic resistance in prostate cancer. 

Highlighted Publications

Qiu, Y., Ravi, L. and Kung, H-J. 1998. Requirement of erbB2 for activation of MAP kinase by Interleukin-6 in Prostate Cancer cells. Nature, 393: 83-85.

Qiu, Y., Robinson, D., Pretlow, T. and Kung, H-J. 1998. Etk, a tyrosine kinase with a PH domain, is an effector of PI3 Kinase and involved in IL6 induced neuroendocrine differentiation of prostate cancer cells. Proc. Natl. Acad. Sci., 95: 3644-3649.

Chen, R., Kim, O., Li, M., Xiong, X., Guan, J-L., Kung, H-J., Chen, H., Shimizu, Y. and Qiu, Y. 2001. Regulation of the PH-domain-containing tyrosine kinase Etk by Focal Adhesion Kinase through the FERM Domain. Nature Cell Biology, 3: 439-444.

Jiang, T., Guo, Z., Dai, B., Kang, M., Ann, D. K., Kung, H-J. and Qiu, Y. 2004. Bi-directional Regulation between Tyrosine Kinase Etk/BMX and Tumor Suppressor p53 in Response to DNA Damage. J. Biol. Chem., 279: 50181 - 50189.

Xie, Y., Xu, K., Dai, B., Guo, Z., Jiang, T., Chen, H. and Qiu, Y. 2006. The 44 kd Pim-1 Kinase Directly Interacts with Tyrosine Kinase Etk/BMX and Protects Human Prostate Cancer Cells from Apoptosis Induced by Chemotherapeutic Drugs. Oncogene 25, 70-78.

Dai, B., Kim, O., Xie, Y., Guo, Z., Xu, K., Kong, X., Melamed, J., Chen, H., Bieberich, C.J., Borowsky, A.D., Kung, HJ, Wei, G., Ostrowski, M.C., Brodie, A., and Qiu, Y. 2006. Tyrosine Kinase Etk/Bmx Is Upregulated in Human Prostate Cancer and Its Overexpression Induces Prostate Intraepithelial Neoplasia in Mouse. Cancer Research 66: 8058-8064.

Guo, Z., Dai, B., Jiang, T., Xu, K., Xie, Y., Kim, O., Nesheiwat, I., Kong, X., Melamed, J., Handratta, V.D., Njar, V.C.O., Brodie, A.M.H., Yu, LR, Veenstra,T.D., Chen, H., and Qiu, Y. 2006. Regulation of Androgen Receptor by Tyrosine Phosphorylation. Cancer Cell, 10:309-319.
Xie, Y, Xu, K, Linn, D., Guo, Z., Nakanishi, T., Ross, D., Chen, H., Fazli, L., Gleave, M. E. and Qiu, Y. 2008. The 44 kDa Pim-1 kinase phosphorylates BCRP/ABCG2 and promotes its drug resistant activity in human prostate cancer cells. J. Biol. Chem., 283:3349-56.
Guo Z., Yang X., Sun F., Jiang R, Linn DE, Chen H, Chen H., Kong X, Melamed J, Tepper CG, Kung H-J, Brodie AMH, Edwards J, and Qiu, Y.  A Novel Androgen Receptor Splice Variant Is Up-regulated during Prostate Cancer Progression and Promotes Androgen Depletion-Resistant Growth. Cancer Research, 69: 2305-13, 2009.
Xu, K., Shimelis, H., Linn, DE., Jiang, R., Yang, X., Sun, F., Guo, Z., Chen, H., Li, W., Chen, H., Kong, X., Melamed, J., Fang, S., Xiao, Z., Veenstra, TD., and Qiu, Y. Regulation of Androgen Receptor Transcriptional Activity and Specificity by RNF6-induced Ubiquitination. Cancer Cell, 15: 270-282, 2009.

Dai, B., Chen H-G., Guo, S., Yang X., Sun F., Linn DE, Li, W., Guo Z., Kong X, Melamed J, Qiu, S, Chen H., and Qiu, Y.  2010. Compensatory up-regulation of tyrosine kinase Etk/BMX in response to androgen deprivation promotes castration-resistant growth of prostate cancer cells. Cancer Res, 70, 5587-5596.

Yang, X. Guo, Z., Sun, F., Li, W., Alfano, A., Shimelis, H, Chen, M., Brodie, AMH., Chen, H., Xiao,Z., Veenstra, TD., and Qiu, Y. 2011 Novel membrane-associated androgen receptor splice variant potentiates proliferative and survival responses in prostate cancer cells. J. Biol. Chem., 286:36152-60.

Sun, F, Chen, HG, Li, W, Yang, X, Wang, X, Jiang, R, Guo, Z,  Chen, H, Huang, J, Borowsky, AD, Qiu, Y. 2014 Androgen receptor splice variant AR3 promotes prostate cancer via modulating expression of  autocrine/paracrine factors. J. Biol. Chem., 289: 1529-1539.

Research Interests

Our research is focused on elucidating molecular mechanisms underlying therapeutic resistance in prostate cancer. We have a long standing interest in the role of post-translational modifications, such as phosphorylation and ubiquitination, in regulation of signaling process in prostate cancer cells. Our lab has demonstrated that posttranslational modifications of the androgen receptor (AR), such as phosphorylation by tyrosine kinases (SRC and ETK/BMX) and ubiquitination by the ubiquitin E3 ligase RNF6, may alter the transcription activity and specificity of AR and lead to resistance to hormonal therapy in prostate cancer.  More recently, our lab has identified several novel splicing variants of AR that are overexpressed in hormone resistant prostate cancer. Expression of AR3 (a.k.a AR-V7), one of the major AR splicing variants, has been shown to correlate with the risk of tumor recurrence and e=resistance to hormone thearpy. We have also established a number of genetic modified mouse models for prostate cancer including ETK and AR variant transgenic models. Dr. Qiu is the co-inventers of two issued US patents on usage of AR splice variants as therapeutic targets and biomarkers. 

Lab Techniques and Equipment

Cell culture and transfection; Molecular cloning and site mutagenesis; real-time PCR, Immunoprecipitation and Western blot; ChIP assays, Immunocytochemistry; Transgenic mouse models; In vivo tumor models; Yeast two-hybrid system; Microarrays