Hailiang Hu

Positions:

Assistant Professor of Pathology

Pathology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

Ph.D. 2000

Shanghai Institute of Biochemistry, Chinese Academy of Sciences

Grants:

Publications:

Targeting cellular heterogeneity with CXCR2 blockade for the treatment of therapy-resistant prostate cancer.

Hormonal therapy targeting androgen receptor (AR) is initially effective to treat prostate cancer (PCa), but it eventually fails. It has been hypothesized that cellular heterogeneity of PCa, consisting of AR+ luminal tumor cells and AR- neuroendocrine (NE) tumor cells, may contribute to therapy failure. Here, we describe the successful purification of NE cells from primary fresh human prostate adenocarcinoma based on the cell surface receptor C-X-C motif chemokine receptor 2 (CXCR2). Functional studies revealed CXCR2 to be a driver of the NE phenotype, including loss of AR expression, lineage plasticity, and resistance to hormonal therapy. CXCR2-driven NE cells were critical for the tumor microenvironment by providing a survival niche for the AR+ luminal cells. We demonstrate that the combination of CXCR2 inhibition and AR targeting is an effective treatment strategy in mouse xenograft models. Such a strategy has the potential to overcome therapy resistance caused by tumor cell heterogeneity.
Authors
Li, Y; He, Y; Butler, W; Xu, L; Chang, Y; Lei, K; Zhang, H; Zhou, Y; Gao, AC; Zhang, Q; Taylor, DG; Cheng, D; Farber-Katz, S; Karam, R; Landrith, T; Li, B; Wu, S; Hsuan, V; Yang, Q; Hu, H; Chen, X; Flowers, M; McCall, SJ; Lee, JK; Smith, BA; Park, JW; Goldstein, AS; Witte, ON; Wang, Q; Rettig, MB; Armstrong, AJ; Cheng, Q; Huang, J
MLA Citation
Li, Yanjing, et al. “Targeting cellular heterogeneity with CXCR2 blockade for the treatment of therapy-resistant prostate cancer..” Sci Transl Med, vol. 11, no. 521, Dec. 2019. Pubmed, doi:10.1126/scitranslmed.aax0428.
URI
https://scholars.duke.edu/individual/pub1423084
PMID
31801883
Source
pubmed
Published In
Sci Transl Med
Volume
11
Published Date
DOI
10.1126/scitranslmed.aax0428

Integration of Transforming Growth Factor   and RAS Signaling Silences a RAB5 Guanine Nucleotide Exchange Factor and Enhances Growth Factor-Directed Cell Migration

Authors
Hu, H; Milstein, M; Bliss, JM; Thai, M; Malhotra, G; Huynh, LC; Colicelli, J
MLA Citation
Hu, H., et al. “Integration of Transforming Growth Factor   and RAS Signaling Silences a RAB5 Guanine Nucleotide Exchange Factor and Enhances Growth Factor-Directed Cell Migration.” Molecular and Cellular Biology, vol. 28, no. 5, American Society for Microbiology, Mar. 2008, pp. 1573–83. Crossref, doi:10.1128/mcb.01087-07.
URI
https://scholars.duke.edu/individual/pub1345126
Source
crossref
Published In
Molecular and Cellular Biology
Volume
28
Published Date
Start Page
1573
End Page
1583
DOI
10.1128/mcb.01087-07

RIN1 Is an ABL Tyrosine Kinase Activator and a Regulator of Epithelial-Cell Adhesion and Migration

Authors
Hu, H; Bliss, JM; Wang, Y; Colicelli, J
MLA Citation
Hu, Hailiang, et al. “RIN1 Is an ABL Tyrosine Kinase Activator and a Regulator of Epithelial-Cell Adhesion and Migration.” Current Biology, vol. 15, no. 9, Elsevier BV, May 2005, pp. 815–23. Crossref, doi:10.1016/j.cub.2005.03.049.
URI
https://scholars.duke.edu/individual/pub1345127
Source
crossref
Published In
Current Biology : Cb
Volume
15
Published Date
Start Page
815
End Page
823
DOI
10.1016/j.cub.2005.03.049

ATM–Dependent MiR-335 Targets CtIP and Modulates the DNA Damage Response

Authors
Martin, NT; Nakamura, K; Davies, R; Nahas, SA; Brown, C; Tunuguntla, R; Gatti, RA; Hu, H
MLA Citation
Martin, Nathan T., et al. “ATM–Dependent MiR-335 Targets CtIP and Modulates the DNA Damage Response.” Plos Genetics, vol. 9, no. 5, Public Library of Science (PLoS), pp. e1003505–e1003505. Crossref, doi:10.1371/journal.pgen.1003505.
URI
https://scholars.duke.edu/individual/pub1345003
Source
crossref
Published In
Plos Genet
Volume
9
Start Page
e1003505
End Page
e1003505
DOI
10.1371/journal.pgen.1003505

Correction to: N-Myc promotes therapeutic resistance development of neuroendocrine prostate cancer by differentially regulating miR-421/ ATM pathway.

Following publication of the original article [1], the authors reported that name that appeared in published online version is incorrect. Aifeng Wang should be Aifen Wang. Corrected name is provided in the author group section above.
Authors
Yin, Y; Xu, L; Chang, Y; Zeng, T; Chen, X; Wang, A; Groth, J; Foo, W-C; Liang, C; Hu, H; Huang, J
MLA Citation
Yin, Yu, et al. “Correction to: N-Myc promotes therapeutic resistance development of neuroendocrine prostate cancer by differentially regulating miR-421/ ATM pathway..” Mol Cancer, vol. 18, no. 1, June 2019. Pubmed, doi:10.1186/s12943-019-1034-y.
URI
https://scholars.duke.edu/individual/pub1393498
PMID
31217018
Source
pubmed
Published In
Molecular Cancer
Volume
18
Published Date
Start Page
107
DOI
10.1186/s12943-019-1034-y