Bin‐Zhi Qian

Fudan University Shanghai Cancer Center

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Jeffrey W. Pollard

University of Edinburgh

Rachel B. Hazan

Albert Einstein College of Medicine

Kimita Suyama

Albert Einstein College of Medicine

Olivier Loudig

Hackensack Meridian Health

Jiufeng Li

Nanjing University

Georgia Agiostratidou

Albert Einstein College of Medicine

Boumediene Bouzahzah

University Medical Center

Maomi Li

Albert Einstein College of Medicine

Inés Badano

National University of Misiones

Eliseo A. Eugenín

The University of Texas Medical Branch at Galveston

Cooperative Institutions

University of Edinburgh

Shanghai Jiao Tong University

Albert Einstein College of Medicine

Queen's Medical Centre

Edinburgh Cancer Research

Medical Research Council

Fudan University

Centre for Inflammation Research

Shanghai Sixth People's Hospital

MRC Institute of Genetics and Molecular Medicine

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Supplementary Figure 1 from Myeloid WNT7b Mediates the Angiogenic Switch and Metastasis in Breast Cancer

Eun-Jin Yeo Luca Cassetta Bin‐Zhi Qian Ian Lewkowich Jiufeng Li

PDF file - 2729K, S1: Flow sorting of human and mouse tumor-associated macrophages.

10.1158/0008-5472.22398996.v1

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Data from Proangiogenic Contribution of Adiponectin toward Mammary Tumor Growth In vivo

Shira Landskroner-Eiger Bin‐Zhi Qian Eric S. Muise Andrea R. Nawrocki Joel P. Berger

<div>AbstractPurpose: Adipocytes represent one of the most abundant constituents of the mammary gland. They are essential for mammary tumor growth and survival. Metabolically, one of the more important fat-derived factors (“adipokines”) is adiponectin (APN). Serum concentrations of APN negatively correlate with body mass index and insulin resistance. To explore the association of APN with breast cancer and tumor angiogenesis, we took an in vivo approach aiming to study its role in the mouse mammary tumor virus (MMTV)-polyoma middle T antigen (PyMT) mammary tumor model.Experimental Design: We compared the rates of tumor growth in MMTV-PyMT mice in wild-type and APN-null backgrounds.Results: Histology and micro-positron emission tomography imaging show that the rate of tumor growth is significantly reduced in the absence of APN at early stages. PyMT/APN knockout mice exhibit a reduction in their angiogenic profile resulting in nutrient deprivation of the tumors and tumor-associated cell death. Surprisingly, in more advanced malignant stages of the disease, tumor growth develops more aggressively in mice lacking APN, giving rise to a larger tumor burden, an increase in the mobilization of circulating endothelial progenitor cells, and a gene expression fingerprint indicative of more aggressive tumor cells.Conclusions: These observations highlight a novel important contribution of APN in mammary tumor development and angiogenesis, indicating that APN has potent angio-mimetic properties in tumor vascularization. However, in tumors deprived of APN, this antiangiogenic stress results in an adaptive response that fuels tumor growth through mobilization of circulating endothelial progenitor cells and the development of mechanisms enabling massive cell proliferation despite a chronically hypoxic microenvironment.</div>

Mammary tumor

10.1158/1078-0432.c.6516858.v1

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Jeffrey W. Pollard (1950–2023)

Immunity (2023)

Bin‐Zhi Qian Johanna A. Joyce

10.1016/j.immuni.2023.05.016

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AR activates YAP/TAZ differentially in prostate cancer

Life Science Alliance (2023)

Omar Salem Siyang Jia Bin‐Zhi Qian Carsten Gram Hansen

The Hippo signalling pathway is a master regulator of cell growth, proliferation, and cancer. The transcriptional coregulators of the Hippo pathway, YAP and TAZ, are central in various cancers. However, how YAP and TAZ get activated in most types of cancers is not well understood. Here, we show that androgens activate YAP/TAZ via the androgen receptor (AR) in prostate cancer (PCa), and that this activation is differential. AR regulates YAP translation while inducing transcription of the TAZ encoding gene, WWTR1 . Furthermore, we show that AR-mediated YAP/TAZ activation is regulated by the RhoA GTPases transcriptional mediator, serum response factor (SRF). Importantly, in prostate cancer patients, SRF expression positively correlates with TAZ and the YAP/TAZ target genes CYR61 and CTGF . We demonstrate that YAP/TAZ are not essential for sustaining AR activity, however, targeting YAP/TAZ or SRF sensitize PCa cells to AR inhibition in anchorage-independent growth conditions. Our findings dissect the cellular roles of YAP, TAZ, and SRF in prostate cancer cells. Our data emphasize the interplay between these transcriptional regulators and their roles in prostate tumorigenesis and highlight how these insights might be exploited therapeutically.

Hippo signaling pathway

CYR61

Mediator

10.26508/lsa.202201620

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Citations (9)

Bufalin suppresses the migration and invasion of prostate cancer cells through HOTAIR, the sponge of miR-520b

Acta Pharmacologica Sinica (2019)

Jianjun Zhang Xiaohui Zhou Yan Zhou Yonggang Wang Bin‐Zhi Qian

Bufalin

HOTAIR

DU145

10.1038/s41401-019-0234-8

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Citations (50)

Abstract 2967: CCL3 autocrine signaling regulate retention of metastasis associated macrophages and promote breast cancer metastasis

Cancer Research (2012)

Bin‐Zhi Qian Takanori Kitamura Jeffrey W. Pollard

Abstract Macrophages abundantly found in the tumor microenvironment enhance malignancy. At metastatic sites a distinct population of metastasis associated macrophages (MAMs) promotes tumor cell extravasation, seeding and persistent growth. These macrophages are derived from circulating inflammatory monocytes recruited by CCL2/CCR2 chemokine signaling. Our current study identified a distinct gene expression signature of the MAMs in comparison with resident macrophages in lung and spleen. Majority of these genes encodes cell surface proteins and secreted factors which mediate MAM's interaction with the metastatic microenvironment. Interestingly, we identified another chemokine, CCL3, is highly expressed by MAMs in a CCL2/CCR2 dependent manner. This indicates that CCL2 not only regulate MAM recruitment but also its function. RNA interference mediated CCL3 knockdown significantly reduced their potential in promoting tumor cell extravasation in vitro. Anti-CCL3 antibody and genetic ablation of CCL3 significantly reduced tumor cell metastatic potential in vivo. Importantly, MAM also express high level of CCR1 and CCR5, receptors for CCL3, upon differentiation. Anti-CCL3 inhibitory antibody significantly reduced MAM retention in pulmonary metastasis. Together, our data indicates an autocrine signaling via CCL3 regulated by CCL2/CCR2 controls MAM retention and promote breast tumor lung metastasis which identified a novel therapeutic target for treating metastatic breast disease. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2967. doi:1538-7445.AM2012-2967

CCL3

CCR2

10.1158/1538-7445.am2012-2967

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Citations (2)

Supplementary Figure 6 from Loss of Retinal Cadherin Facilitates Mammary Tumor Progression and Metastasis

Georgia Agiostratidou Maomi Li Kimita Suyama Inés Badano Rinat Keren

Supplementary Figure 6 from Loss of Retinal Cadherin Facilitates Mammary Tumor Progression and Metastasis

Mammary tumor

Tumor progression

10.1158/0008-5472.22378458

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MYC sensitises cells to apoptosis by driving energetic demand

Nature Communications (2022)

Joy Edwards-Hicks Huizhong Su Maurizio Mangolini Kubra K Yoneten Jimi Wills

Abstract The MYC oncogene is a potent driver of growth and proliferation but also sensitises cells to apoptosis, which limits its oncogenic potential. MYC induces several biosynthetic programmes and primary cells overexpressing MYC are highly sensitive to glutamine withdrawal suggesting that MYC-induced sensitisation to apoptosis may be due to imbalance of metabolic/energetic supply and demand. Here we show that MYC elevates global transcription and translation, even in the absence of glutamine, revealing metabolic demand without corresponding supply. Glutamine withdrawal from MRC-5 fibroblasts depletes key tricarboxylic acid (TCA) cycle metabolites and, in combination with MYC activation, leads to AMP accumulation and nucleotide catabolism indicative of energetic stress. Further analyses reveal that glutamine supports viability through TCA cycle energetics rather than asparagine biosynthesis and that TCA cycle inhibition confers tumour suppression on MYC-driven lymphoma in vivo. In summary, glutamine supports the viability of MYC-overexpressing cells through an energetic rather than a biosynthetic mechanism.

Catabolism

10.1038/s41467-022-32368-z

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Citations (21)

New tricks for metastasis-associated macrophages

Breast Cancer Research (2012)

Bin‐Zhi Qian Jeffrey W. Pollard

Recent studies on breast cancer lung metastasis have identified a new mechanism of tumor cell survival via signaling provided by metastasis-associated macrophages. Targeting these specialized host immune cells and their specific signals provides an attractive and potential therapeutic approach for treating the disease.

Surgical oncology

10.1186/bcr3143

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Citations (26)

Data from Myeloid WNT7b Mediates the Angiogenic Switch and Metastasis in Breast Cancer

Eun-Jin Yeo Luca Cassetta Bin‐Zhi Qian Ian Lewkowich Jiufeng Li

<div>AbstractOncogenic targets acting in both tumor cells and tumor stromal cells may offer special therapeutic appeal. Interrogation of the Oncomine database revealed that 52 of 53 human breast carcinomas showed substantial upregulation of WNT family ligand WNT7B. Immunolabeling of human mammary carcinoma showed that WNT7B immunoreactivity was associated with both tumor cells and with tumor-associated macrophages. In the MMTV-PymT mouse model of mammary carcinoma, we found tumor progression relied upon WNT7B produced by myeloid cells in the microenvironment. Wnt7b deletion in myeloid cells reduced the mass and volume of tumors due to a failure in the angiogenic switch. In the tumor overall, there was no change in expression of Wnt/β-catenin pathway target genes, but in vascular endothelial cells (VEC), expression of these genes was reduced, suggesting that VECs respond to Wnt/β-catenin signaling. Mechanistic investigations revealed that failure of the angiogenic switch could be attributed to reduced Vegfa mRNA and protein expression in VECs, a source of VEGFA mRNA in the tumor that was limiting in the absence of myeloid WNT7B. We also noted a dramatic reduction in lung metastasis associated with decreased macrophage-mediated tumor cell invasion. Together, these results illustrated the critical role of myeloid WNT7B in tumor progression, acting at the levels of angiogenesis, invasion, and metastasis. We suggest that therapeutic suppression of WNT7B signaling might be advantageous due to targeting multiple aspects of tumor progression. Cancer Res; 74(11); 2962–73. ©2014 AACR.</div>

10.1158/0008-5472.c.6505200.v1

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