Margaret Liu

Jiujiang University

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Lufang Zhou

University of Alabama at Birmingham

Yingnan Si

The Ohio State University

Seulhee Kim

The Ohio State University

Jiashuai Zhang

The Ohio State University

Kai Chen

Zhejiang Institute of Communications

Ashley George

The Ohio State University

Z“

Zhuoxin “Zora” Zhou

The Ohio State University

Jianfa Ou

University of Alabama at Birmingham

Runhua Liu

Beijing University of Chinese Medicine

Patrick Erñst

University of Zurich

Cooperative Institutions

University of Alabama at Birmingham

119

Johns Hopkins University

National Institutes of Health

Chinese Academy of Sciences

University of Pennsylvania

The Ohio State University

Daewoong Pharmaceutical (South Korea)

Huazhong University of Science and Technology

University of Alabama

Nanjing Medical University

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Data from Loss of FOXP3 and TSC1 Accelerates Prostate Cancer Progression through Synergistic Transcriptional and Posttranslational Regulation of c-MYC

Lianpin Wu Baozhu Yi Shi Wei Dapeng Rao Youhua He

<div>AbstractAlthough c-MYC and mTOR are frequently activated proteins in prostate cancer, any interaction between the two is largely untested. Here, we characterize the functional cross-talk between FOXP3–c-MYC and TSC1–mTOR signaling during tumor progression. Deletion of Tsc1 in mouse embryonic fibroblasts (MEF) decreased phosphorylation of c-MYC at threonine 58 (pT58) and increased phosphorylation at serine 62 (pS62), an observation validated in prostate cancer cells. Conversely, inhibition of mTOR increased pT58 but decreased pS62. Loss of both FOXP3 and TSC1 in prostate cancer cells synergistically enhanced c-MYC expression via regulation of c-Myc transcription and protein phosphorylation. This crosstalk between FOXP3 and TSC1 appeared to be mediated by both the mTOR–4EBP1–c-MYC and FOXP3–c-MYC pathways. In mice, Tsc1 and Foxp3 double deletions in the prostate led to prostate carcinomas at an early age; this did not occur in these mice with an added c-Myc deletion. In addition, we observed synergistic antitumor effects of cotreating mice with inhibitors of mTOR and c-MYC in prostate cancer cells and in Foxp3 and Tsc1 double-mutant mice. In human prostate cancer, loss of nuclear FOXP3 is often accompanied by low expression of TSC1. Because loss of FOXP3 transcriptionally induces c-Myc expression and loss of TSC1 activates mTOR signaling, these data suggest cross-talk between FOXP3–c-MYC and TSC1–mTOR signaling that converges on c-MYC to regulate tumor progression. Coadministration of c-MYC and mTOR inhibitors may overcome the resistance to mTOR inhibition commonly observed in prostate cancer cells.Significance:These results establish the principle of a synergistic action of TSC1 and FOXP3 during prostate cancer progression and provide new therapeutic targets for patients who have prostate cancer with two signaling defects.</div>

Post-translational regulation

TSC1

10.1158/0008-5472.c.6511659

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[Comparison of the latest cancer statistics, cancer epidemic trends and determinants between China and the United States].

PubMed (2024)

Young-Min Ji S W Liu Y M Zhang Haiyan Duan Margaret Liu

To provide supports for the cancer prevention and control strategies in China by comparing the disease burden, epidemic trends, 5-year relative survival rate and major determinants of common cancers between China and the United States.

10.3760/cma.j.cn112152-20240208-00068

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Supplementary Figure S5 from A Dual-Payload Antibody–Drug Conjugate Targeting CD276/B7-H3 Elicits Cytotoxicity and Immune Activation in Triple-Negative Breast Cancer

Zhuoxin “Zora” Zhou Yingnan Si Jiashuai Zhang Kai Chen Ashley George

Supplementary Figure S5

Triple-negative breast cancer

Conjugate

Antibody-drug conjugate

Payload (computing)

10.1158/0008-5472.27755486

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Table S1 from A Dual-Payload Antibody–Drug Conjugate Targeting CD276/B7-H3 Elicits Cytotoxicity and Immune Activation in Triple-Negative Breast Cancer

Zhuoxin “Zora” Zhou Yingnan Si Jiashuai Zhang Kai Chen Ashley George

Supplementary Table S1

Triple-negative breast cancer

Antibody-drug conjugate

Conjugate

Payload (computing)

10.1158/0008-5472.27837703

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Cell Populations and Known Surface Antigens of Tumors Induced by Abelson Virus in Pristane-Primed BALB/c Mice: An Analysis by Immunoelectron Microscopy 2

JNCI Journal of the National Cancer Institute (1975)

Tadao Aoki Michael Potter Macie M. Sturm Margaret Liu Mary Jane Walling

When Abelson murine leukemia virus (MuLV-A) was inoculated into pristane-primed BALB/c mice, either plasmacytomas (PCT), lymphosarcomas, or their mixed form was induced with a shorter latent period than that for PCT induction in mice treated with pristane alone. All 3 neoplasms were designated Abelson's tumors. The morphology of the induced malignant cells and the presence of known surface antigens were analyzed by electron microscopy. The cell surface antigens (CSA) examined were PC1, X.1, Gross (GCSA), and Moloney (MCSA); viral envelope antigens (VEA) were xVEA, x1-VEA, sub-gsVEA, and MVEA. MuLV-A-pristane-induced PCT cells produced markedly fewer intracisternal type-A particles than did mineral oil-induced PCT cells. Most, if not all, mineral oil-induced PCT cells carried PC1 antigen and produced many extracellular type-C viruses carrying xVEA and x1-VEA, whereas Abelson's tumor cells had both a lower incidence and a smaller amount of PC1 and X.1 antigens and xVEA+ virus and lacked x1-VEA+ virus. In addition, most Abelson's tumors and their type-C viruses did not carry MCSA and MVEA ro GCSA and sub-gsVEA. All the macrophages in the PC1+ Abelson's tumors and many macrophages in PC1-Abelson's tumors contained various amounts of PC1 on their cell surfaces. For these reasons, Abelson's tumors were clearly distinct from pristane- or mineral oil-induced BALB/c PCT and from M-MuLV- ro G-MuLV-induced tumors.

Immunoelectron microscopy

BALB/c

10.1093/jnci/55.5.1097

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Crystal structure of (3R)-Hydroxyacyl-Acyl Carrier Protein Dehydratase (FabZ) from Helicobacter pylori in complex with compound 3i

L. Zhang Lipeng He Margaret Liu H. Liu X. Shen

Porphobilinogen synthase

Crystal (programming language)

10.2210/pdb2glm/pdb

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Data for EMSL Project 60182 from March 2023

OSTI OAI (U.S. Department of Energy Office of Scientific and Technical Information) (2023)

Diane M. Beckles Margaret Liu Tamar Krugman Arnold J. Bloom

10.25582/data.2023-03.2770754/2325934

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β-Blockade Affects Simulator Scores

Ophthalmology (2011)

Renelle Pointdujour Habeeb Ahmad Margaret Liu Edward R. Smith Douglas R. Lazzaro

10.1016/j.ophtha.2011.04.019

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Citations (14)

Targeted Extracellular Vesicles Delivered Verrucarin A to Treat Glioblastoma

Biomedicines (2022)

Kai Chen Yingnan Si Jia-Shiung Guan Zhuoxin “Zora” Zhou Seulhee Kim

Glioblastomas, accounting for approximately 50% of gliomas, comprise the most aggressive, highly heterogeneous, and malignant brain tumors. The objective of this study was to develop and evaluate a new targeted therapy, i.e., highly potent natural compound verrucarin A (Ver-A), delivered with monoclonal antibody-directed extracellular vesicle (mAb-EV). First, the high surface expression of epidermal growth factor receptor (EGFR) in glioblastoma patient tissue and cell lines was confirmed using immunohistochemistry staining, flow cytometry, and Western blotting. mAb-EV-Ver-A was constructed by packing Ver-A and tagging anti-EGFR mAb to EV generated from HEK293F culture. Confocal microscopy and the In Vivo Imaging System demonstrated that mAb-EV could penetrate the blood-brain barrier, target intracranial glioblastoma xenografts, and deliver drug intracellularly. The in vitro cytotoxicity study showed IC

MTT assay

10.3390/biomedicines10010130

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Characterization of iPSCs derived from low grade gliomas revealed early regional chromosomal amplifications during gliomagenesis

Journal of Neuro-Oncology (2018)

Zhong Liu Pulin Che Juan J. Mercado James R. Hackney Gregory K. Friedman

10.1007/s11060-018-03047-1

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Citations (12)