Boyang (Jason) Wu

Education

PhD in molecular pharmacology and toxicology, University of Southern California, Los Angeles, Calif., 2009

Bachelor of Science in biochemistry, Hong Kong University of Science and Technology, Hong Kong, China, 2004

Professional Training & Experience

Assistant professor, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, Calif., 2015-2016

Project scientist, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, Calif., 2014-2016

Postdoctoral researcher, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, Calif., 2010-2014

Research

The role of neuromimicry in cancer metastasis
Tumor cells have the ability to disseminate from the primary site and to establish metastatic deposits at distant sites, and vascular and lymphatic channels have become well-accepted routes of metastatic spread. By contrast, another route of tumor spread that occurs in and along nerves has received inadequate attention. We and other groups have recently shown that prostate cancer cells develop neuromimicry by expressing neuronal genes and exhibiting neuron-like phenotypes, enabling cancer cells to mimic and reciprocally interact with nerves and thus promote cancer spread in and along nerves to initiate metastasis. We have identified aberrant expression of select neurotrophic and axon guidance genes in a cohort of prostate cancer patients. Using xenograft mouse models and 3-dimentional cell co-culture models, we focus on exploring how these neuronal genes induce cancer neuromimicry to promote tumor-nerve crosstalk and thus perineural invasion/metastasis. We are also interested in developing pharmacological targeting strategies to interfere with tumor-nerve communications, aiming for inhibiting nerve-facilitated cancer metastasis.

Molecular characterization of tumor-stromal interactions
It has become well-recognized that cancer cells do not act autonomously when they establish either the primary tumor or metastatic deposits at different organs. Rather, intricate interactions between tumor cells and their stromal microenvironment play an essential role in tumor initiation and metastasis. We will use a multidisciplinary approach, combining a series of in vitro and in vivo model systems with integrative genomic technologies, to identify and validate novel genes and pathways mediating molecular crosstalks between tumor cells and resident stromal cells. By leveraging the power of profiling tools to analyze both available clinical genomic profiling data of human cancers and our own collection of tumor-stromal cell pairs, we are particularly interested in elucidating how tumor-stromal interactions affect intrinsic stemness and plasticity features of a specialized group of cells named tumor-/metastasis-initiating cells in tumor initiation, recurrence and metastasis.

Molecular understanding of androgen receptor signaling and antiandrogen resistance in castration-resistant and neuroendocrine prostate cancer
Androgen receptor pathway targeted therapy is the current treatment regimen for castration-resistant prostate cancer and its metastatic form, which are leading causes of morbidity and mortality in men with advanced prostate cancer. Recent introduction of new potent androgen receptor pathway inhibitors, such as enzalutamide and abiraterone acetate, into clinical arena is expected to shape castration-resistant prostate cancer treatment landscapes for the next decade. However, the emergence of resistance to antiandrogen agents represents a major clinical challenge. We are interested in identifying and characterizing novel genes that interact with androgen receptor and contribute to the development of antiandrogen resistance by using genomic and proteomic profiling approaches in established castration-resistant and antiandrogen-resistant prostate cancer cells. We will also develop rational monotherapeutic and/or combination treatment strategies to overcome antiandrogen resistance. Additionally, we aim to extend our studies to other aggressive phenotype of prostate cancer selectively induced by highly potent antiandrogens, such as neuroendocrine prostate cancer, and dissect the mechanisms underlying the pathogenesis of neuroendocrine prostate cancer.

Selected Peer-Reviewed Publications

Li J, Pu T, Yin L, Li Q, Liao CP, Wu BJ. (2020) MAOA-mediated reprogramming of stromal fibroblasts promotes prostate tumorigenesis and cancer stemness. Oncogene, 39(16):3305-21.

Wang R, Chu GC, Wang X, Wu JB, Hu P, Multani AS, Pathak S, Zhau HE, Chung LW. (2019) Establishment and characterization of a prostate cancer cell line from a prostatectomy specimen for the study of cellular interaction. International Journal of Cancer, 145(8): 2249-59.

Lin TP, Li J, Li Q, Li X, Liu C, Zeng N, Huang JM, Chu GC, Lin CH, Zhau HE, Chung LW, Wu BJ*, Shih JC*. (2018) R1 regulates prostate tumor growth and progression by transcriptional suppression of the E3 ligase HUWE1 to stabilize c-Myc. (*co-corresponding author) Molecular Cancer Research, 16(12):1940-51.

Yin L, Li J, Liao CP, Wu BJ. (2018) Monoamine oxidase deficiency causes prostate atrophy and reduces prostate progenitor cell activity. Stem Cells, 36(8):1249-58.

Wu JB*, Yin L, Shi C, Li Q, Duan P, Huang JM, Liu C, Wang F, Lewis M, Wang Y, Lin TP, Pan CC, Posadas EM, Zhau HE, Chung LW*. (2017) MAOA-dependent activation of sonic hedgehog-IL6-RANKL signaling network promotes prostate cancer metastasis by engaging tumor-stromal cell interactions. (*co-corresponding author) Cancer Cell, 31(3):368-82. (Featured Article)

Liu S, Tian Z, Zhang L, Hou S, Hu S, Wu J, Jing Y, Sun H, Yu F, Zhao L, Wang R, Tseng HR, Zhau HE, Chung LW, Wu K, Wang H*, Wu JB*, Nie Y*, Shao C*. (2016) Combined cell surface carbonic anhydrase 9 and CD147 antigens enable high-efficiency capture of circulating tumor cells in clear cell renal cell carcinoma patients. (*co-corresponding author) Oncotarget 7(37):59877-91.

Zhao N, Zhang C, Zhao Y, Bai B, An J, Zhang H, Wu JB*, Shi C*. (2016) Optical imaging of gastric cancer with near-infrared heptamethine carbocyanine fluorescence dyes. (*co-corresponding author) Oncotarget 7(35):57277-89.

Wu JB*, Shi C*, Chu GC, Xu Q, Zhang Y, Li Q, Yu JS, Zhau HE, Chung LW. (2015) Near-infrared fluorescence heptamethine carbocyanine dyes mediate imaging and targeted drug delivery for brain tumor. (*equal contribution) Biomaterials 67:1-10.

Wu JB, Lin TP, Gallagher JD, Kushal S, Chung LW, Zhau HE, Olenyuk BZ, Shih JC. (2015) Monoamine oxidase A inhibitor − near-infrared dye conjugate reduces prostate tumor growth. J Am Chem Soc 137(6):2366-74. (Cover Article)

Wu JB*, Shao C*, Li X, Shi C, Li Q, Hu P, Chen YT, Dou X, Sahu D, Li W, Harada H, Zhang Y, Wang R, Zhau HE, Chung LW. (2014) Near-infrared fluorescence imaging of cancer mediated by tumor hypoxia and HIF1α/OATPs signaling axis. (*equal contribution) Biomaterials 35(28):8175-85.

Wu JB, Shao C, Li X, Li Q, Hu P, Shi C, Li Y, Chen YT, Yin F, Liao CP, Zhau HE, Shih JC, Chung LW. (2014) Monoamine oxidase A mediates prostate tumorigenesis and cancer metastasis. J Clin Invest 124(7):2891-908.

Wu JB, Shih JC. (2011) Valproic acid induces monoamine oxidase A via Akt/Fockhead Box 1 activation. Mol Pharmacol 80(4):714-23.

Wu JB, Chen K, Li Y, Lau YF, Shih JC. (2009) Regulation of monoamine oxidase A by the SRY gene on the Y chromosome. FASEB J 23(11):4029-38.

Wu JB, Chen K, Ou XM, Shih JC. (2009) Retinoic acid activates monoamine oxidase B promoter in human neuronal cells. J Biol Chem 284(25):16723-35.

Book Chapters

Wu JB, Chung LW. (2015) The PI3K-mTOR pathway in prostate cancer: biological significance and therapeutic opportunities. In: PI3K-mTOR in Cancer and Cancer Therapy pp 263-289. Ed. Leyland-Jones B, De P, Dey N. (Springer Press)

Additional Information

Current funding support: National Institutes of Health and Department of Defense