Qionghua Zhu

Southern University of Science and Technology

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Walter Birchmeier

Max Delbrück Center

William I. Weis

Stanford University

Edgar Specker

Leibniz-Forschungsinstitut für Molekulare Pharmakologie

Jens Peter von Kries

Leibniz-Forschungsinstitut für Molekulare Pharmakologie

Annika Wulf‐Goldenberg

Helios Hospital Berlin-Buch

Liang Fang

Beijing Academy of Agricultural and Forestry Sciences

Liang Fang

Foshan University

Martin Neuenschwander

Leibniz-Forschungsinstitut für Molekulare Pharmakologie

Martin Neuenschwander

Leibniz-Forschungsinstitut für Molekulare Pharmakologie

Liang Fang

Chongqing Medical University

Cooperative Institutions

Southern University of Science and Technology

Max Delbrück Center

Chinese Academy of Sciences

Charité - Universitätsmedizin Berlin

Zhejiang University

University of Chinese Academy of Sciences

Central South University

Freie Universität Berlin

Berlin Institute of Health at Charité - Universitätsmedizin Berlin

University of Science and Technology of China

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Supplementary Material from A Small-Molecule Antagonist of the β-Catenin/TCF4 Interaction Blocks the Self-Renewal of Cancer Stem Cells and Suppresses Tumorigenesis

Liang Fang Qionghua Zhu Martin Neuenschwander Edgar Specker Annika Wulf‐Goldenberg

Portions of Materials and Methods and Supplementary Tables 1 and 2. Table S1: Primer sequences for ChIP experiment Table S2: Primer sequences for qRT-PCR

Primer (cosmetics)

Table (database)

10.1158/0008-5472.22409421

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Suppressor of cytokine signaling and insulin resistance, leptin resistance

Intern J Endocrinol Metab (2009)

Qionghua Zhu Jingya Li Qiaojun He Bo Yang Jia Li

Suppressor of cytokine signaling (SOCS) are the negative regulators of cytokine signaling via inhibition of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. The family comprises eight structurally homologous members, including CIS (cytokine inducible SH2 containing protein) and SOCS-1 ～7. Current evidence suggests that specific members of the SOCS play a role in the development of leptin and insulin resistance owing to inhibiting leptin and insulin signaling pathways,which results in dysfunction of glucose balance and diabetes. The SOCS proteins inhibit leptin and insulin signaling by influencing multiple proteins, including insulin receptor substrate (IRS), phosphatidylinositol 3-kinase (PI3K) ,JAK leptin receptor (LR),STAT. Key words: Suppressor of cytokine signaling; Insulin resistance; Leptin resistance; Diabetes mellitus

Janus kinase 2

Leptin receptor

IRS2

Insulin receptor substrate

SOCS2

Cytokine receptor

10.3760/cma.j.issn.1673-4157.2009.03.018

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Supplementary Figure 1 from A Small-Molecule Antagonist of the β-Catenin/TCF4 Interaction Blocks the Self-Renewal of Cancer Stem Cells and Suppresses Tumorigenesis

Liang Fang Qionghua Zhu Martin Neuenschwander Edgar Specker Annika Wulf‐Goldenberg

Fig. S1 Technology and protein production for the primary High Throughput Screen (HTS).

10.1158/0008-5472.22409445.v1

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A contraction-reaction-diffusion model for circular pattern formation in embryogenesis

Journal of the Mechanics and Physics of Solids (2021)

Tiankai Zhao Yubing Sun Qionghua Zhu Xin Li Mehdi Baghaee

Reaction–diffusion system

Pattern Formation

10.1016/j.jmps.2021.104630

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A Small-Molecule Antagonist of the β-Catenin/TCF4 Interaction Blocks the Self-Renewal of Cancer Stem Cells and Suppresses Tumorigenesis

Cancer Research (2015)

Liang Fang Qionghua Zhu Martin Neuenschwander Edgar Specker Annika Wulf-Goldenberg

Abstract Wnt/β-catenin signaling is a highly conserved pathway essential for embryogenesis and tissue homeostasis. However, deregulation of this pathway can initiate and promote human malignancies, especially of the colon and head and neck. Therefore, Wnt/β-catenin signaling represents an attractive target for cancer therapy. We performed high-throughput screening using AlphaScreen and ELISA techniques to identify small molecules that disrupt the critical interaction between β-catenin and the transcription factor TCF4 required for signal transduction. We found that compound LF3, a 4-thioureido-benzenesulfonamide derivative, robustly inhibited this interaction. Biochemical assays revealed clues that the core structure of LF3 was essential for inhibition. LF3 inhibited Wnt/β-catenin signals in cells with exogenous reporters and in colon cancer cells with endogenously high Wnt activity. LF3 also suppressed features of cancer cells related to Wnt signaling, including high cell motility, cell-cycle progression, and the overexpression of Wnt target genes. However, LF3 did not cause cell death or interfere with cadherin-mediated cell–cell adhesion. Remarkably, the self-renewal capacity of cancer stem cells was blocked by LF3 in concentration-dependent manners, as examined by sphere formation of colon and head and neck cancer stem cells under nonadherent conditions. Finally, LF3 reduced tumor growth and induced differentiation in a mouse xenograft model of colon cancer. Collectively, our results strongly suggest that LF3 is a specific inhibitor of canonical Wnt signaling with anticancer activity that warrants further development for preclinical and clinical studies as a novel cancer therapy. Cancer Res; 76(4); 891–901. ©2015 AACR.

TCF4

10.1158/0008-5472.can-15-1519

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The Wnt-Driven Mll1 Epigenome Regulates Salivary Gland and Head and Neck Cancer

Cell Reports (2019)

Qionghua Zhu Liang Fang Julian Heuberger Andrea Kranz Jörg Schipper

We identified a regulatory system that acts downstream of Wnt/β-catenin signaling in salivary gland and head and neck carcinomas. We show in a mouse tumor model of K14-Cre-induced Wnt/β-catenin gain-of-function and Bmpr1a loss-of-function mutations that tumor-propagating cells exhibit increased Mll1 activity and genome-wide increased H3K4 tri-methylation at promoters. Null mutations of Mll1 in tumor mice and in xenotransplanted human head and neck tumors resulted in loss of self-renewal of tumor-propagating cells and in block of tumor formation but did not alter normal tissue homeostasis. CRISPR/Cas9 mutagenesis and pharmacological interference of Mll1 at sequences that inhibit essential protein-protein interactions or the SET enzyme active site also blocked the self-renewal of mouse and human tumor-propagating cells. Our work provides strong genetic evidence for a crucial role of Mll1 in solid tumors. Moreover, inhibitors targeting specific Mll1 interactions might offer additional directions for therapies to treat these aggressive tumors.

Epigenome

10.1016/j.celrep.2018.12.059

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Citations (22)

Supplementary Figure Legends from A Small-Molecule Antagonist of the β-Catenin/TCF4 Interaction Blocks the Self-Renewal of Cancer Stem Cells and Suppresses Tumorigenesis

Liang Fang Qionghua Zhu Martin Neuenschwander Edgar Specker Annika Wulf‐Goldenberg

Supplementary figure legends

TCF4

10.1158/0008-5472.22409424

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RUNX Proteins as Epigenetic Modulators in Cancer

Cells (2022)

Hongyang Yi Yuhao He Qionghua Zhu Liang Fang

RUNX proteins are highly conserved in metazoans and perform critical functions during development. Dysregulation of RUNX proteins through various molecular mechanisms facilitates the development and progression of various cancers, where different RUNX proteins show tumor type-specific functions and regulate different aspects of tumorigenesis by cross-talking with different signaling pathways such as Wnt, TGF-β, and Hippo. Molecularly, they could serve as transcription factors (TFs) to activate their direct target genes or interact with many other TFs to modulate chromatin architecture globally. Here, we review the current knowledge on the functions and regulations of RUNX proteins in different cancer types and highlight their potential role as epigenetic modulators in cancer.

10.3390/cells11223687

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Citations (9)

Wnt/β-catenin signalling induces MLL to create epigenetic changes in salivary gland tumours

The EMBO Journal (2013)

Peter Wend Liang Fang Qionghua Zhu Jörg Schipper Christoph Loddenkemper

Beta-catenin

H3K4me3

10.1038/emboj.2013.127

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Citations (90)

Supplementary Figure 6 from A Small-Molecule Antagonist of the β-Catenin/TCF4 Interaction Blocks the Self-Renewal of Cancer Stem Cells and Suppresses Tumorigenesis