Microenvironmental regulation of epithelial-mesenchymal transitionsin cancer

Research output: Contribution to journalArticle

Dingcheng Gao, Linda T. Vahdat, Stephen T. Wong, Jenny C. Chang, Vivek Mittal

The evolution of the cancer cell into a metastatic entity is the major cause of death in patients with cancer. Activation of the epithelial-to- mesenchymal transition (EMT) endows invasive and metastatic properties upon cancer cells that favor successful colonization of distal target organs. The observation that in many cancers distant metastases resemble the epithelial phenotype of primary tumors has led to speculation that the disseminated tumor cells recruited to the target organs undergo mesenchymal-to-epithelial transition (MET). However, the MET cascade has not been recapitulated in vivo, and the cellular and molecular regulators that promote MET remain unknown. In a recent report, using a model of spontaneous breast cancer, we have shown that bone marrow-derived myeloid progenitor cells in the premetastatic lung secrete the proteoglycan versican, which induces MET of metastatic tumor cells and accelerates metastases. This review summarizes recent progress in MET research, outlines a unique paracrine cross-talk between the microenvironment and the cancer cells, which promotes tumor outgrowth in the metastatic organ, and discusses opportunities for novel antimetastatic approaches for cancer therapy.

Original languageEnglish
Pages (from-to)4883-4889
Number of pages7
JournalCancer Research
Volume72
Issue number19
DOIs
StatePublished - Oct 1 2012

PMID: 23002209

PMCID: PMC3649848

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Microenvironmental regulation of epithelial-mesenchymal transitionsin cancer. / Gao, Dingcheng; Vahdat, Linda T.; Wong, Stephen T.; Chang, Jenny C.; Mittal, Vivek.

In: Cancer Research, Vol. 72, No. 19, 01.10.2012, p. 4883-4889.

Research output: Contribution to journalArticle

Harvard

Gao, D, Vahdat, LT, Wong, ST, Chang, JC & Mittal, V 2012, 'Microenvironmental regulation of epithelial-mesenchymal transitionsin cancer' Cancer Research, vol. 72, no. 19, pp. 4883-4889. https://doi.org/10.1158/0008-5472.CAN-12-1223

APA

Gao, D., Vahdat, L. T., Wong, S. T., Chang, J. C., & Mittal, V. (2012). Microenvironmental regulation of epithelial-mesenchymal transitionsin cancer. Cancer Research, 72(19), 4883-4889. https://doi.org/10.1158/0008-5472.CAN-12-1223

Vancouver

Gao D, Vahdat LT, Wong ST, Chang JC, Mittal V. Microenvironmental regulation of epithelial-mesenchymal transitionsin cancer. Cancer Research. 2012 Oct 1;72(19):4883-4889. https://doi.org/10.1158/0008-5472.CAN-12-1223

Author

Gao, Dingcheng ; Vahdat, Linda T. ; Wong, Stephen T. ; Chang, Jenny C. ; Mittal, Vivek. / Microenvironmental regulation of epithelial-mesenchymal transitionsin cancer. In: Cancer Research. 2012 ; Vol. 72, No. 19. pp. 4883-4889.

BibTeX

@article{deaf17469b35452383c09da6c94a1086,
title = "Microenvironmental regulation of epithelial-mesenchymal transitionsin cancer",
abstract = "The evolution of the cancer cell into a metastatic entity is the major cause of death in patients with cancer. Activation of the epithelial-to- mesenchymal transition (EMT) endows invasive and metastatic properties upon cancer cells that favor successful colonization of distal target organs. The observation that in many cancers distant metastases resemble the epithelial phenotype of primary tumors has led to speculation that the disseminated tumor cells recruited to the target organs undergo mesenchymal-to-epithelial transition (MET). However, the MET cascade has not been recapitulated in vivo, and the cellular and molecular regulators that promote MET remain unknown. In a recent report, using a model of spontaneous breast cancer, we have shown that bone marrow-derived myeloid progenitor cells in the premetastatic lung secrete the proteoglycan versican, which induces MET of metastatic tumor cells and accelerates metastases. This review summarizes recent progress in MET research, outlines a unique paracrine cross-talk between the microenvironment and the cancer cells, which promotes tumor outgrowth in the metastatic organ, and discusses opportunities for novel antimetastatic approaches for cancer therapy.",
author = "Dingcheng Gao and Vahdat, {Linda T.} and Wong, {Stephen T.} and Chang, {Jenny C.} and Vivek Mittal",
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RIS

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AU - Wong, Stephen T.

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AU - Mittal, Vivek

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AB - The evolution of the cancer cell into a metastatic entity is the major cause of death in patients with cancer. Activation of the epithelial-to- mesenchymal transition (EMT) endows invasive and metastatic properties upon cancer cells that favor successful colonization of distal target organs. The observation that in many cancers distant metastases resemble the epithelial phenotype of primary tumors has led to speculation that the disseminated tumor cells recruited to the target organs undergo mesenchymal-to-epithelial transition (MET). However, the MET cascade has not been recapitulated in vivo, and the cellular and molecular regulators that promote MET remain unknown. In a recent report, using a model of spontaneous breast cancer, we have shown that bone marrow-derived myeloid progenitor cells in the premetastatic lung secrete the proteoglycan versican, which induces MET of metastatic tumor cells and accelerates metastases. This review summarizes recent progress in MET research, outlines a unique paracrine cross-talk between the microenvironment and the cancer cells, which promotes tumor outgrowth in the metastatic organ, and discusses opportunities for novel antimetastatic approaches for cancer therapy.

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