Jieya Shao, PhD


jieya-shaoI received my BS degree in Biochemistry from Nankai University in China, after which I came to the US to pursue my PhD degree in the laboratory of Dr. Robert Matts at the Oklahoma State University. The focus of my PhD work was on the regulation of protein kinase folding and maturation by heat shock proteins. Curious about translational research involving human diseases, I next joined Dr. Marc Diamond’s laboratory in the Neurology Department at the University of California, San Francisco School of Medicine to study protein misfolding diseases with a specific focus on Huntington disorder for my postdoctoral training. While characterizing a novel huntingtin modifier named Profilin-1, I was fascinated by the long-standing paradox of Profilin-1 being both an essential gene and a tumor suppressor which, despite making little sense to me at the time, pulled me into the complex world of cancer biology. Changing field on my own was by no means easy, but incredibly fulfilling. After finishing my postdoctoral training, I joined the Oncology Division at Washington University and worked for two years under the supervision of Dr. Matthew Ellis, the experience of which further solidified my long-term interest in mechanism-driven cancer research. It was also during this period that I developed strong interest in cancer treatment resistance mechanisms particularly with regard to chemotherapies. Currently an Associate Professor, I am running my laboratory in the Oncology Division of the Department of Medicine.


As a curiosity-driven lab, we are broadly interested in uncovering novel and clinically relevant drivers and targets of cancer with the overarching goal of improving patient outcome. Currently, our major research effort is directed towards understanding the mechanisms of action and therapeutic potentials of two multi-functional proteins, the actin-binding protein Profilin-1 and the AAA+ ATPase p97/VCP, in the contexts of genome stability maintenance and cancer chemotherapy efficacy. Both are essential proteins with complicated cellular functions intricately regulated by subcellular localization, protein-protein interactions, and post-translational modifications. It is our ultimate goal that mechanistic insights from such studies may reveal hidden “Achilles heels” of DNA damage response machineries of cancer cells, and guide the development of novel and personalized cancer therapies.

Shao Research

Lab website: www.shaolab.org

Recent publications

  1. Zhu C, Iwase M, Li Z, Wang F, Quinet A, Vindigni A, Shao J. Profilin-1 Regulates DNA Replication Forks in a Context-Dependent Fashion by Interacting with SNF2H and BOD1L. Nature Communications, 2022 Nov 1;13(1):6531.
  2. Wang F, Vij K, Li L, Dodhiawala P, Lim KH, Shao J. Phospho-Ser784-VCP drives resistance of pancreatic ductal adenocarcinoma to genotoxic chemotherapies and predicts chemo-sensitizing effect of VCP inhibitor. Cancers, 2021 Oct 11;13(20):5076.
  3. Wang F, Zhu C, Cai S, Boudreau A, Kim S, Bissell MJ, Shao J. Ser71 phosphorylation inhibits actin-binding of profilin-1 and its apoptosis-sensitizing activity. Front Cell Dev Biol. 2021; 9:692269.
  4. Zhu C*, Kim S*, Mooradian A, Wang F, Li Z, Holohan S, Collins P, Wang K, Guo Z, Hoog J, Ma CX, Oltz EM, Held JM, Shao J. Cancer-Associated Exportin-6 Upregulation Inhibits the Transcriptionally Repressive and Anticancer Effects of Nuclear Profilin-1. (*Equal Contribution) Cell Rep. 2021; 34(7):108749.
  5. Shao J. Ser784 phosphorylation: a clinically relevant enhancer of VCP function in the DNA damage response. Mol Cell Oncol. 2020; 7(5):1796179.
  6. Zhu C*, Rogers A*, Asleh K*, Won J, Gao D, Leung S, Li S, Vij KR, Zhu J, Held JM, You Z, Nielsen TO, Shao J. Phospho-Ser784-VCP Is Required for DNA Damage Response and Is Associated With Poor Prognosis of Chemotherapy-Treated Breast Cancer. (*Equal Contribution). Cell Rep. 2020; 31(10):107745.
  7. Lei J*, Shao J*, Zhang J*, Iglesia M*, Chan CW, Cao J, Anurag M, Singh P, He X, Kosaka Y, Matsunuma R, Crowder R, Hoog J, Phommaly C, Goncalves R, Ramalho S, Peres RM, Punturi N, Schmidt C, Bartram A, Jou E, DevarakondaV, Holloway KR, Lai W, Hampton O, Rogers A, Tobias E, Parikh P, Davies SR, Li S, Ma CX, Suman V, Hunt K, Watson M, Hoadley KA, Thompson A, Chen X, Kavuri SM, Creighton CJ, Maher C, Perou C, Haricharan S, Ellis MJ. Functional annotation of ESR1 gene fusions in estrogen receptor positive breast cancer. (*Equal Contribution) Cell Rep. 2018; 24(6):1434-1444.
  8. Diamond MI, Cai S, Boudreau A, Carey CJ Jr, Lyle N, Pappu RV, Swamidass SJ, Bissell M, Piwnica-Worms H, Shao J. Subcellular localization and Ser-137 phosphorylation regulate tumor-suppressive activity of profilin-1. J Biol Chem. 2015;290(14):9075-9086.
  9. Li S*, Shen D*, Shao J, Crowder R, Liu W, Prat A, He X, Liu S, Hoog J, Lu C, Ding L, Griffith OL, Miller C, Larson D, Fulton RS, Harrison M, Mooney T, McMichael JF, Luo J, Tao Y, Goncalves R, Schlosberg C, Hiken JF, Saied L, Sanchez C, Giuntoli T, Bumb C, Cooper C, Kitchens RT, Lin A, Phommaly C, Davies SR, Zhang J, Kavuri MS, McEachern D, Dong YY, Ma C, Pluard T, Naughton M, Bose R, Suresh R, McDowell R, Michel L, Aft R, Gillanders W, DeSchryver K, Wilson RK, Wang S, Mills GB, Gonzalez-Angulo A, Edwards JR, Maher C, Perou CM, Mardis ER, Ellis MJ. Endocrine-therapy-resistant ESR1 variants revealed by genomic characterization of breast-cancer-derived xenografts. (*Equal Contribution) Cell Rep. 2013;4(6):1116-1130.
  10. Shao J, Welch WJ, Diprospero NA, Diamond MI. Phosphorylation of profilin by ROCK1 regulates polyglutamine aggregation. Mol Cell Biol. 2008; 28(17):5196-5120.