Qiuyang Zhang, PhD

Assistant Professor, Structural & Cellular Biology

(504) 988-5527
School of Medicine
Qiuyang Zhang, PhD (Lisa)


Dr. Zhang received a bachelor degree in biology from Shaanxi Normal University, China in 1987.  She was appointed assistant professor at Shaanxi University of Chinese Medicine in 1987 and was promoted to lecturer in 1994 and associate professor in 2002.  Dr. Zhang received a master of science degree in 2001 and a PhD degree in 2004 from Xi’an Jiaotong University School of Medicine and then joined the faculty there as an associate professor in the Department of Anatomy and Histology and Embryology.  In 2005, she started her postdoctoral training in molecular biology at Eastern New Mexico University and then in cancer genetics at Loyola University in Chicago.  In 2006, Dr. Zhang joined George Washington University as a research scientist in the Department of Biochemistry and Molecular Biology.  In 2009, she joined Tulane University School of Medicine as a postdoctoral fellow in molecular cancer biology in the Department of Structural & Cellular Biology.  She was promoted to be an instructor in 2014 and assistant professor in 2018.  Dr. Zhang’s research interests include reproductive biology, cancer biology, and inflamm-aging. 
Research Programs:
1) Aging and Prostate Cancer: Dr. Zhang has a long-standing interest in prostate cancer, particularly in aging’s contribution to prostate carcinogenesis and the efficacies of candidate aging-associated prostate cancer interventions. The incidence of prostate cancer rises rapidly with increasing age beginning around 50, with the highest rates seen in those aged 70 to 80. Optimal management of prostate cancer in the elderly (> 75 years) remains a significant clinical challenge. Low-grade inflammation (i.e., inflammaging) plays an essential role in the aging process, and chronic inflammation contributes to the onset and progression of prostate cancer.  Inflammaging is often attributed to the progressive activation of immune cells. In that regard, a disruption in the balance of pro-inflammatory CD4+ T helper (Th) 17 cells and homeostatic regulatory T (Treg) cell responses in favor of Th17 cells has been reported in non-cancer-related aging humans and mice. More recent evidence has suggested a similar imbalance between Th17 and Treg as a prominent factor in cancer development; however, the mechanisms by which aging influences the balance of Th17 and Treg, and the extent to which an imbalance contributes to initiation and progression of prostate cancer, are unclear. We are currently working on (1) identifying associations between Th17/Treg ratio alteration and human PCa progression associated with advanced aging; (2) defining how aging-associated imbalances in the Th17/Treg axis drive PCa; and (3) determining the efficacy of therapeutic targeting of Th17/Treg axis in preventing age-associated PCa.   An R01 grant (R01CA255802) supported this project.
2) Ubiquitin-specific protease 26 (USP26) and Prostate Cancer: Androgen deprivation therapy (ADT) remains the first-line therapy for advanced PCa.  Still, treatment resistance inevitably develops and leads to an abysmal prognosis of stage-castration resistant PCa (CRPC). Therefore, there is an urgent need to develop strategies for the prevention/treatment of CRPC by targeting specific factors essential for tumor survival instead of targeting AR signaling. USP26 is a member of deubiquitinases (DUBs) involved in various cellular functions and plays a vital role in cancer development. We are currently generating prostate-specific Usp26 knockout mouse models using CRISP/Cas9 techniques to elucidate the role of USP26 in PCa.
3) USP26 and Male Infertility: USP26 is mainly expressed in testis. Mutations in this gene have been associated with Sertoli cell-only syndrome and male infertility. My team studied the single nucleotide polymorphisms (SNPs) of USP26 in infertile male patients compared to normal males (Asian J Androl. 2007; Asian J Androl. 2009). We have generated an Usp26 KO mouse model, the first of its kind, and found that disruption of Usp26 causes male subfertility associated with spermatogenesis defects in mice (Biol Reprod. 2019). We are currently working on generating testis-specific Usp26 knockout mice to elucidate the mechanisms of USP26 in spermatogenesis and sperm maturation.


Liu S, Zhang B, Rowan BG, Jazwinski SM, Abdel-Mageed AB, Steele C, Wang AR, Sartor O, Niu T, Zhang Q. A Novel Controlled PTEN-Knockout Mouse Model for Prostate Cancer Study. Front Mol Biosci. 2021;8:696537. doi: 10.3389/fmolb.2021.696537. eCollection 2021. PubMed PMID: 34150854; PubMed Central PMCID: PMC8211560.

Liu S, Liu F, Zhang B, Yan P, Rowan BG, Abdel-Mageed AB, Steele C, Jazwinski SM, Moroz K, Norton EB, Wang A, Myers L, Sartor O, Zhang Q. CD4+ T helper 17 cell response of aged mice promotes prostate cancer cell migration and invasion. Prostate. 2020 Jul;80(10):764-776. doi: 10.1002/pros.23990. Epub 2020 May 1. PubMed PMID: 32356608; PubMed Central PMCID: PMC7310589.

Tian H, Huo Y, Zhang J, Ding S, Wang Z, Li H, Wang L, Lu M, Liu S, Qiu S, Zhang Q. Disruption of ubiquitin specific protease 26 gene causes male subfertility associated with spermatogenesis defects in mice†. Biol Reprod. 2019 Apr 1;100(4):1118-1128. doi: 10.1093/biolre/ioy258. PubMed PMID: 30561524; PubMed Central PMCID: PMC6698735.

Zhang Q, Liu S, Parajuli KR, Zhang W, Zhang K, Mo Z, Liu J, Chen Z, Yang S, Wang AR, Myers L, You Z. Interleukin-17 promotes prostate cancer via MMP7-induced epithelial-to-mesenchymal transition. Oncogene. 2017 Feb 2;36(5):687-699. doi: 10.1038/onc.2016.240. Epub 2016 Jul 4. PubMed PMID: 27375020; PubMed Central PMCID: PMC5213194.

Zhang Q, Liu S, Ge D, Zhang Q, Xue Y, Xiong Z, Abdel-Mageed AB, Myers L, Hill SM, Ro-wan BG, Sartor O, Melamed J, Chen Z, You Z. Interleukin-17 promotes formation and growth of prostate adenocarcinoma in mouse models. Cancer Res. 2012 May 15;72(10):2589-99. doi: 10.1158/0008-5472.CAN-11-3795. Epub 2012 Mar 28. PubMed PMID: 22461511; PubMed Central PMCID: PMC3665158. Featured on the cover of the May 15, 2012 issue.

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Inflamm-aging and prostate cancer