Jiaoti Huang
· Johnston-West Distinguished Professor of PathologyVerifiedDuke University · Pathology
Active 1989–2026
About
Dr. Jiaoti Huang is the Johnston-West Distinguished Professor of Pathology, Chair Professor of Pathology, Professor of Pharmacology and Cancer Biology, and Professor of Cell Biology at Duke University School of Medicine. He is also a member of the Duke Cancer Institute. Dr. Huang's laboratory primarily focuses on the study of prostate cancer, investigating various aspects such as cellular heterogeneity contributing to hormone therapy resistance and disease progression, metabolic mechanisms involved in carcinogenesis and cell survival, and novel therapeutic approaches for treating castration-resistant prostate cancer. His research is translational, closely related to human disease, and benefits from a multidisciplinary expertise in molecular and cellular biology, biochemistry, animal models, histology, and immunohistochemistry, as well as access to extensive tissue resources including archival and fresh prostate cancer specimens. A major area of specialization in Dr. Huang's lab is the study of neuroendocrine (NE) cells in prostate cancer. These cells, which lack androgen receptor expression and are androgen-independent, survive and become enriched after hormonal therapy, contributing to castration resistance. His lab was the first to report that NE cells express CXCR2 and GPC3, leading to the development of novel therapeutic agents and ongoing clinical trials targeting this therapy-resistant tumor cell population. Another key research focus is the metabolic mechanisms underlying prostate cancer progression. Dr. Huang's lab has identified that prostate cancer cells become "addicted" to glutamine for survival during hormonal therapy due to an isoform switch in glutaminase (GLS1), and inhibition of the potent isoform Glutaminase C strongly suppresses tumor growth, informing drug development efforts. Additionally, Dr. Huang's research addresses the significant inter- and intra-tumoral heterogeneity of prostate cancer, which is a major mechanism of therapy resistance. Using advanced sequencing technologies, his lab identifies subpopulations of tumor cells responsible for disease progression and evolutionary relationships between these populations. This work has led to the discovery of minor cell populations inherently resistant to hormonal therapy and novel markers that may predict therapy responsiveness and patient survival. Overall, Dr. Huang's research integrates molecular, cellular, and clinical insights to advance understanding and treatment of advanced and therapy-resistant prostate cancer.
Research topics
- Medicine
- Internal medicine
- Biology
- Cancer research
- Genetics
- Pathology
- Oncology
- Artificial Intelligence
- Radiology
- Computer Science
- Biochemistry
- Bioinformatics
- Cell biology
- Surgery
- Nuclear medicine
Selected publications
A probe of the maximum energetics of fast radio bursts through a prolific repeating source
University of Groningen research database (University of Groningen / Centre for Information Technology) · 2026-01-01 · 7 citations
articleOpen accessFast radio bursts (FRBs) are sufficiently energetic to be detectable from luminosity distances up to at least seven billion parsecs (redshift z > 1). Probing the maximum energies and luminosities of FRBs constrains their emission mechanism and cosmological population. Here, we investigate the maximum energetics of a highly active repeater, FRB 20220912A, using 1500h of observations. We detect 130 high-energy bursts and find a break in the burst energy distribution, with a flattening of the power-law slope at higher energy – consistent with the behaviour of another highly active repeater, FRB 20201124A. There is a roughly equal split of integrated burst energy between the low- and high-energy regimes. Furthermore, we model the rate of the highest energy bursts and find a turnover at a characteristic spectral energy density of E<sup>char</sup><sub>v</sub> = 2.09<sup>+3.78</sup><sub>-1.04</sub> × 10<sup>32</sup> ergHz<sup>-1</sup>. This characteristic maximum energy agrees well with observations of apparently one-off FRBs, suggesting a common physical mechanism for their emission. The extreme burst energies push radiation and source models to their limit: at this burst rate a typical magnetar (B = 10<sup>15</sup> G) would deplete the energy stored in its magnetosphere in ∼2150h, assuming a radio efficiency ϵ<sub>radio</sub> = 10<sup>-5</sup>. We find that the high-energy bursts (E<sub>v</sub> > 3 × 10<sup>30</sup> ergHz<sup>-1</sup>) play an important role in exhausting the energy budget of the source.
A HyperFlash and ÉCLAT view of the local environment and energetics of the repeating FRB 20240619D
Monthly Notices of the Royal Astronomical Society · 2026-01-20 · 1 citations
preprintOpen accessABSTRACT Time-variable propagation effects provide a window into the local plasma environments of repeating fast radio burst (FRB) sources. Here we report high-cadence observations of FRB 20240619D, as part of the HyperFlash and ÉCLAT programmes. We observed for 500 h and detected 217 bursts, including 10 bursts with high fluence ($&gt;25$ Jy ms) and implied energy. We track burst-to-burst variations in dispersion measure (DM) and rotation measure (RM), from which we constrain the parallel magnetic field strength in the source’s local environment: $0.27\pm 0.13$ mG. Apparent DM variations between sub-bursts in a single bright event are interpreted as coming from plasma lensing or variable emission height. We also identify two distinct scintillation screens along the line of sight, one associated with the Milky Way and the other likely located in the FRB’s host galaxy or local environment. Together, these (time-variable) propagation effects reveal that FRB 20240619D is embedded in a dense, turbulent and highly magnetised plasma. The source’s environment is more dynamic than that measured for many other (repeating) FRB sources, but less extreme compared to several repeaters that are associated with a compact, persistent radio source. FRB 20240619D’s cumulative burst fluence distribution shows a power-law break, with a flat tail at high energies. Along with previous studies, this emphasises a common feature in the burst energy distribution of hyperactive repeaters. Using the break in the burst fluence distribution, we estimate a source redshift of $z=0.042-0.240$ . We discuss FRB 20240619D’s nature in the context of similar studies of other repeating FRBs.
2025-11-24
articleOpen access<p>Supplemental Movies 2a-2c: 22Rv1-NuclightGreen and SHP-77-NuclightRed mixed population co-cultures. Time-lapse movies of 22Rv1 cells (labeled with NuclightGreen) and SHP-77 cells (labeled with NuclightRed) co-cultured with T cells. Both the 22Rv1 and SHP-77 cells were plated at equal densities and treated with either NT control BiTE®, AMG 757, or the PSMA-targeting HLE BiTE, AMG 160. T cells were added to each well at an E:T ratio of 10:1. Images were captured every 4 hours at 4x magnification for 5 days. a. 22Rv1, SHP-77, and T cells co-cultured with NT control BiTE®. b. 22Rv1, SHP-77, and T cells co-cultured with AMG 757. c. 22Rv1, SHP-77, and T cells co-cultured with AMG 160.</p>
2025-11-24
articleOpen access<p>Supplemental Movies 1a-1d: 22Rv1-LacZ and 22Rv1-DLL3 cells co-cultures. Time-lapse movies of 22Rv1-LacZ and 22Rv1-DLL3 cells (labeled with NuclightRed) co-cultured with T cells and either NT control BiTE® or AMG 757. T cells were plated at an E:T ratio of 5:1. Images were captured every 6 hours at 10x magnification. a. 22Rv1-LacZ cells and T cells treated with NT control BiTE®. b. 22Rv1-DLL3 cells and T cells treated with NT control BiTE®. c. 22Rv1-LacZ cells and T cells treated with AMG 757. d. 22Rv1-DLL3 cells and T cells treated with AMG 757.</p>
2025-11-24
articleOpen access<p>FigureS8</p>
2025-11-24
articleOpen access<p>Supplemental Movies 1a-1d: 22Rv1-LacZ and 22Rv1-DLL3 cells co-cultures. Time-lapse movies of 22Rv1-LacZ and 22Rv1-DLL3 cells (labeled with NuclightRed) co-cultured with T cells and either NT control BiTE® or AMG 757. T cells were plated at an E:T ratio of 5:1. Images were captured every 6 hours at 10x magnification. a. 22Rv1-LacZ cells and T cells treated with NT control BiTE®. b. 22Rv1-DLL3 cells and T cells treated with NT control BiTE®. c. 22Rv1-LacZ cells and T cells treated with AMG 757. d. 22Rv1-DLL3 cells and T cells treated with AMG 757.</p>
bioRxiv (Cold Spring Harbor Laboratory) · 2025-11-13
preprintOpen accessAbstract Prostate cancer (PC) remains the second leading cause of cancer-related mortality in men. The emergence of treatment-emergent neuroendocrine prostate cancer (NEPC) arising from androgen receptor (AR) pathway inhibition poses a significant clinical challenge. Here, we report that NUAK family kinase 2 (NUAK2) is an actionable therapeutic target in NEPC. NUAK2 expression is markedly elevated in NEPC patient specimens and preclinical models, and its genetic or pharmacologic inhibition suppresses NEPC tumor growth. The FDA-approved CDK4/6 inhibitor trilaciclib exerts potent inhibition of NUAK2, leading to marked tumor suppression alone and enhanced efficacy in combination with carboplatin. Integrated phospho-target and interactome analyses demonstrate that NUAK2 engages core spliceosome components to regulate pre-mRNA splicing. As proof of principle, we validated that NUAK2 inhibition perturbs pre-mRNA splicing of EZH2 and TTK leading to reduced translation. Collectively, these findings establish NUAK2 as a clinically actionable regulator of RNA splicing and tumor progression in NEPC, revealing a novel mechanism by which trilaciclib exerts antitumor activity in NEPC. Graphical Abstract
2025-11-24
articleOpen access<p>Supplemental Movies 1a-1d: 22Rv1-LacZ and 22Rv1-DLL3 cells co-cultures. Time-lapse movies of 22Rv1-LacZ and 22Rv1-DLL3 cells (labeled with NuclightRed) co-cultured with T cells and either NT control BiTE® or AMG 757. T cells were plated at an E:T ratio of 5:1. Images were captured every 6 hours at 10x magnification. a. 22Rv1-LacZ cells and T cells treated with NT control BiTE®. b. 22Rv1-DLL3 cells and T cells treated with NT control BiTE®. c. 22Rv1-LacZ cells and T cells treated with AMG 757. d. 22Rv1-DLL3 cells and T cells treated with AMG 757.</p>
2025-11-24
articleOpen access<p>FigureS10</p>
2025-11-24
articleOpen access<p>FigureS6</p>
Recent grants
Role of oncogenic phosphorylated MED1 in aggressive prostate cancer
NIH · $1.6M · 2017–2022
Role of oncogenic phosphorylated MED1 in aggressive prostate cancer
NIH · $387k · 2017–2022
Role and targeting of PRMT5 in prostate cancer
NIH · $2.4M · 2017–2023
NIH · $1.9M · 2018
NIH · $271k · 2021
Frequent coauthors
- 158 shared
Owen N. Witte
- 131 shared
Qi Yang
University of Chinese Academy of Sciences
- 130 shared
David G. Wagner
University of Nebraska Medical Center
- 128 shared
Paula Sochacki
John D. Dingell VA Medical Center
- 128 shared
Qazi Rais Ahmed
- 128 shared
Nagi F. Khouri
UPMC Health System
- 128 shared
Glynis Scott
University of Rochester Medical Center
- 128 shared
Victor Holguín Prieto
Washington University in St. Louis
Labs
Education
- 1990
Ph.D., Biochemistry
New York University
- 1983
MD
Anhui Medical University
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