Zhong Chen

Positions:

Assistant Professor in Pathology

Pathology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

Ph.D. 2008

Peking Union Medical College (China)

Grants:

Publications:

Re: Diverse AR-V7 Cistromes in Castration-Resistant Prostate Cancer are Governed by HoxB13.

Authors
Atala, A
MLA Citation
Atala, Anthony. “Re: Diverse AR-V7 Cistromes in Castration-Resistant Prostate Cancer are Governed by HoxB13.J Urol, vol. 201, no. 3, Mar. 2019, pp. 446–47. Pubmed, doi:10.1097/01.JU.0000553716.75971.4e.
URI
https://scholars.duke.edu/individual/pub1404143
PMID
30759678
Source
pubmed
Published In
The Journal of Urology
Volume
201
Published Date
Start Page
446
End Page
447
DOI
10.1097/01.JU.0000553716.75971.4e

Integrative analysis identifies targetable CREB1/FoxA1 transcriptional co-regulation as a predictor of prostate cancer recurrence.

Authors
Sunkel, B; Wu, D; Chen, Z; Wang, C-M; Liu, X; Ye, Z; Horning, AM; Liu, J; Mahalingam, D; Lopez-Nicora, H; Lin, C-L; Goodfellow, PJ; Clinton, SK; Jin, VX; Chen, C-L; Huang, TH-M; Wang, Q
MLA Citation
Sunkel, Benjamin, et al. “Integrative analysis identifies targetable CREB1/FoxA1 transcriptional co-regulation as a predictor of prostate cancer recurrence.Nucleic Acids Res, vol. 45, no. 11, June 2017, p. 6993. Pubmed, doi:10.1093/nar/gkx282.
URI
https://scholars.duke.edu/individual/pub1499328
PMID
28419278
Source
pubmed
Published In
Nucleic Acids Res
Volume
45
Published Date
Start Page
6993
DOI
10.1093/nar/gkx282

Transcriptional regulation of survivin by c-Myc in BCR/ABL-transformed cells: implications in anti-leukaemic strategy.

BCR/ABL can cause chronic myelogenous leukaemia (CML) in part by altering the transcription of specific genes with growth- and/or survival-promoting functions. Recently, BCR/ABL has been shown to activate survivin, an important regulator of cell growth and survival, but the precise molecular mechanisms behind its expression and consequences thereof in CML cells remain unclear. Here, we reported that BCR/ABL promotes survivin expression and its cytoplasmic accumulation. The increase of survivin was largely controlled at the transcriptional level through a mechanism mediated by JAK2/PI3K signal pathways that activated c-Myc, leading to transactivation of survivin promoter. Dynamic down-regulation of survivin was a key event involved in imatinib-induced cell death while forced expression of survivin partially counteracted imatinib's effect on cell survival. Additionally, shRNA-mediated silencing of survivin or c-Myc eradicated colony formation of K562 cells in semi-solid culture system, implying an essential role for this transcriptional network in BCR/ABL-mediated cell transformation and survival. Finally, interruption of c-Myc activity by 10058-F4 exerted an anti-leukaemia effect with a synergistic interaction with imatinib and overcame the anti-apoptosis rescued by IL-3 supplement. In conclusion, we have identified JAK2/PI3K-mediated and c-Myc-dependent transactivation of survivin as a novel pathway in the transcriptional network orchestrated by BCR/ABL. These results suggest that the interference with this circuitry might be a potential utility for CML treatment.
Authors
Fang, ZH; Dong, CL; Chen, Z; Zhou, B; Liu, N; Lan, HF; Liang, L; Liao, WB; Zhang, L; Han, ZC
MLA Citation
Fang, Zhi Hong, et al. “Transcriptional regulation of survivin by c-Myc in BCR/ABL-transformed cells: implications in anti-leukaemic strategy.J Cell Mol Med, vol. 13, no. 8B, Aug. 2009, pp. 2039–52. Pubmed, doi:10.1111/j.1582-4934.2008.00549.x.
URI
https://scholars.duke.edu/individual/pub1499327
PMID
19602047
Source
pubmed
Published In
Journal of Cellular and Molecular Medicine
Volume
13
Published Date
Start Page
2039
End Page
2052
DOI
10.1111/j.1582-4934.2008.00549.x

Overexpression of cell surface cytokeratin 8 in multidrug-resistant MCF-7/MX cells enhances cell adhesion to the extracellular matrix.

Accumulating evidence suggests that multiple complex mechanisms may be involved, simultaneously or complementarily, in the emergence and development of multidrug resistance (MDR) in various cancers. Cell adhesion-mediated MDR is one such mechanism. In the present study, we initially observed increased cell adhesion to extracellular matrix proteins by the MDR human breast tumor cell line MCF-7/MX compared to its parental cells. We then used a strategy that combined antibody-based screening technique and mass spectrometry-based proteomics to identify membrane proteins that contribute to the enhanced adhesion of MCF-7/MX cells. Using MCF-7/MX cells as immunogen, we isolated a mouse monoclonal antibody, 9C6, that preferentially reacts with MCF-7/MX cells over the parental MCF-7 cells. The molecular target of 9C6 was identified as cytokeratin 8 (CK8), which was found to be overexpressed on the cell surface of MCF-7/MX cells. We further observed that down-regulation of cell surface levels of CK8 through siRNA transfection significantly inhibited MCF-7/MX cell adhesion to fibronectin and vitronectin. In addition, anti-CK8 siRNA partially reversed the MDR phenotype of MCF-7/MX cells. Taken together, our results suggest that alterations in the expression level and cellular localization of CK8 may play a significant role in enhancing the cellular adhesion of MDR MCF-7/MX cells.
Authors
Liu, F; Chen, Z; Wang, J; Shao, X; Cui, Z; Yang, C; Zhu, Z; Xiong, D
MLA Citation
Liu, Fang, et al. “Overexpression of cell surface cytokeratin 8 in multidrug-resistant MCF-7/MX cells enhances cell adhesion to the extracellular matrix.Neoplasia, vol. 10, no. 11, Nov. 2008, pp. 1275–84. Pubmed, doi:10.1593/neo.08810.
URI
https://scholars.duke.edu/individual/pub1499330
PMID
18953437
Source
pubmed
Published In
Neoplasia
Volume
10
Published Date
Start Page
1275
End Page
1284
DOI
10.1593/neo.08810

ChemInform Abstract: STAT3: A Critical Transcription Activator in Angiogenesis

Authors
Chen, Z; Han, ZC
MLA Citation
Chen, Zhong, and Zhong Chao Han. “ChemInform Abstract: STAT3: A Critical Transcription Activator in Angiogenesis.” Cheminform, vol. 39, no. 24, Wiley, June 2008. Crossref, doi:10.1002/chin.200824243.
URI
https://scholars.duke.edu/individual/pub1499322
Source
crossref
Published In
Cheminform
Volume
39
Published Date
DOI
10.1002/chin.200824243