Jiaoti Huang

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…

Research topics

• Medicine
• Internal medicine
• Biology
• Cancer research
• Genetics
• Pathology
• Oncology
• Artificial Intelligence
• Radiology
• Computer Science

Selected publications

• The DNA methylation landscape of advanced prostate cancer

  Nature Genetics · 2020 · 348 citations

  DOI

• Transcriptional profiling identifies an androgen receptor activity-low, stemness program associated with enzalutamide resistance

  Proceedings of the National Academy of Sciences · 2020 · 168 citations

  gene alterations and AR expression were similar between groups. Importantly, however, transcriptional measurements demonstrated that specific gene sets-including those linked to low AR transcriptional activity and a stemness program-were activated in nonresponders. Our results suggest that patients whose tumors harbor this program should be considered for clinical trials testing rational agents to overcome de novo enzalutamide resistance.

  DOI

• Targeting therapy-resistant prostate cancer via a direct inhibitor of the human heat shock transcription factor 1

  Science Translational Medicine · 2020 · 85 citations

  gene was amplified, and nuclear HSF1 abundance was markedly increased in prostate cancers and particularly in neuroendocrine prostate cancer (NEPC), for which there are no available treatment options. Despite genetic validation of HSF1 as a therapeutic target in a range of cancers, a direct and selective small-molecule HSF1 inhibitor has not been validated or developed for use in the clinic. We described the identification of a direct HSF1 inhibitor, Direct Targeted HSF1 InhiBitor (DTHIB), which…

  DOI

• Tumor heterogeneity in VHL drives metastasis in clear cell renal cell carcinoma

  Signal Transduction and Targeted Therapy · 2023 · 74 citations

  ) cells, promoted metastasis by enhancing the motility of VHL-WT cells and facilitating tumor cell vascular escape. Genetic deletion or antibody blockade of POSTN dramatically suppressed lung metastases in our preclinical models. This work supports a new strategy to halt the progression of ccRCC by disrupting the critical metastatic crosstalk between heterogeneous cell populations within a tumor.

  PublisherOA PDFDOI

• A glutaminase isoform switch drives therapeutic resistance and disease progression of prostate cancer

  Proceedings of the National Academy of Sciences · 2021 · 72 citations

  Senior authorCorresponding

  Cellular metabolism in cancer is significantly altered to support the uncontrolled tumor growth. How metabolic alterations contribute to hormonal therapy resistance and disease progression in prostate cancer (PCa) remains poorly understood. Here we report a glutaminase isoform switch mechanism that mediates the initial therapeutic effect but eventual failure of hormonal therapy of PCa. Androgen deprivation therapy inhibits the expression of kidney-type glutaminase (KGA), a splicing isoform of gl…

  DOI

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

Frequent coauthors

• Owen N. Witte

  158 shared

• Qi Yang

  University of Chinese Academy of Sciences

  131 shared

• David G. Wagner

  University of Nebraska Medical Center

  130 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

  128 shared

Labs

• Huang LabPI

Education

• Ph.D., Biochemistry

  New York University

  1990

• MD

  Anhui Medical University

  1983

Similar researchers at Duke University

• Soman Ninan Abrahamh-99
• Maureane Hoffmanh-88
• Rex Colle Bentleyh-80