Inhibition of Cyclooxygenase‐2 Suppresses Lymph Node Metastasis via VEGF‐C

Liu, Huidong; Yang, Yanmei; Xiao, Jianbing; Lv, Yanhong; Liu, Yan; Yang, Huiqi; Zhao, Luqing

doi:10.1002/ar.20940

Cited by 20 publications

(17 citation statements)

References 32 publications

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“…In a mice lung cancer model celecoxib, a selective COX2 inhibitor reduced lymphangiogenesis and lymph node metastasis [180] indicating that VEGF expression and thereby lymphangiogenesis might be associated with prostaglandins.…”

Section: Future Immunotherapeutic Strategies To Block Lymphangiogementioning

confidence: 99%

Impact of the Prolymphangiogenic Crosstalk in the Tumor Microenvironment on Lymphatic Cancer Metastasis

Schlereth

Refaian

Iden

et al. 2014

BioMed Research International

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Lymphangiogenesis is a very early step in lymphatic metastasis. It is regulated and promoted not only by the tumor cells themselves, but also by cells of the tumor microenvironment, including cancer associated fibroblasts, mesenchymal stem cells, dendritic cells, or macrophages. Even the extracellular matrix as well as cytokines and growth factors are involved in the process of lymphangiogenesis and metastasis. The cellular and noncellular components influence each other and can be influenced by the tumor cells. The knowledge about mechanisms behind lymphangiogenesis in the tumor microenvironmental crosstalk is growing and offers starting points for new therapeutic approaches.

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Section: Future Immunotherapeutic Strategies To Block Lymphangiogementioning

confidence: 99%

Impact of the Prolymphangiogenic Crosstalk in the Tumor Microenvironment on Lymphatic Cancer Metastasis

Schlereth

Refaian

Iden

et al. 2014

BioMed Research International

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“…Further, increased LVD in the peritumor region correlates with increased metastasis in a number of human cancers, directly implicating new lymphatic vessel formation in tumor cell dissemination (106–108). A multitude of studies have examined mechanisms driving neo-lymphangiogenesis in the breast tumor environment, and VEGF-C, VEGF-D, macrophages, and COX-2/PGE 2 have emerged as key players (51, 68, 72, 73, 80, 99–101, 109–118). …”

Section: Lymphatic Vasculature In Breast Cancer Metastasismentioning

confidence: 99%

Deciphering Pro-Lymphangiogenic Programs during Mammary Involution and Postpartum Breast Cancer

2016

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Postpartum breast cancers are a highly metastatic subset of young women’s breast cancers defined as breast cancers diagnosed in the postpartum period or within 5 years of last child birth. Women diagnosed with postpartum breast cancer are nearly twice as likely to develop metastasis and to die from breast cancer when compared with nulliparous women. Additionally, epidemiological studies utilizing multiple cohorts also suggest that nearly half of all breast cancers in women aged <45 qualify as postpartum cases. Understanding the biology that underlies this increased risk for metastasis and death may lead to identification of targeted interventions that will benefit the large number of young women with breast cancer who fall into this subset. Preclinical mouse models of postpartum breast cancer have revealed that breast tumor cells become more aggressive if they are present during the normal physiologic process of postpartum mammary gland involution in mice. As involution appears to be a period of lymphatic growth and remodeling, and human postpartum breast cancers have high peritumor lymphatic vessel density (LVD) and increased incidence of lymph node metastasis (1, 2), we propose that novel insight into is to be gained through the study of the biological mechanisms driving normal postpartum mammary lymphangiogenesis as well as in the microenvironment of postpartum tumors.

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“…NSAIDs regulate lymphangiogenesis by reducing macrophage secretion of VEGF-C to modulate lymphatic vessel density and by modulating the morphology of lymphatic collector vessels that facilitated metastasis [13, 126, 169, 170]. While most clinical trials involving NSAIDs have emphasized tumour growth, mortality and metastasis, future clinical trials evaluating the efficacy of NSAIDs on tumour metastasis should focus on clinical evaluations of tumour lymphatics.…”

Section: Drugs That Target Angiogenesis and Lymphangiogenesismentioning

confidence: 99%

Lymphovascular and neural regulation of metastasis: Shared tumour signalling pathways and novel therapeutic approaches

Karnezis

Achen

et al. 2013

Best Practice & Research Clinical Anaesthesiology

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The progression of cancer is supported by a wide variety of non-neoplastic cell types which make up the tumour stroma, including immune cells, endothelial cells, cancer-associated fibroblasts and nerve fibres. These host cells contribute molecular signals that enhance primary tumour growth and provide physical avenues for metastatic dissemination. This article provides an overview of the role of blood vessels, lymphatic vessels and nerve fibres in the tumour microenvironment, and highlights the interconnected molecular signalling pathways that control their development and activation in cancer. Further the review highlights the known pharmacological agents which target these pathways and discusses the potential therapeutic uses of drugs that target angiogenesis, lymphangiogenesis and stress response pathways in the different stages of cancer care.

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Inhibition of Cyclooxygenase‐2 Suppresses Lymph Node Metastasis via VEGF‐C

Abstract: Most experimental work addressing cyclooxygenase-2 (COX-2) inhibitor has focused on suppressing hematogenic spread. Little is known about the mechanism by which this inhibitor can also block lymphatic metastasis.

Cited by 20 publications

References 32 publications

Impact of the Prolymphangiogenic Crosstalk in the Tumor Microenvironment on Lymphatic Cancer Metastasis

Impact of the Prolymphangiogenic Crosstalk in the Tumor Microenvironment on Lymphatic Cancer Metastasis

Deciphering Pro-Lymphangiogenic Programs during Mammary Involution and Postpartum Breast Cancer

Lymphovascular and neural regulation of metastasis: Shared tumour signalling pathways and novel therapeutic approaches

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