Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Brief Communications Arising
  • Published:

Upholding a role for EMT in pancreatic cancer metastasis

Nature volume 547, pages E7–E8 (2017)Cite this article

Subjects

arising from X. Zheng et al. Nature 527, 525–530 (2015); doi:10.1038/nature16064

Epithelial-to-mesenchymal transition (EMT) is a cellular program that operates in the context of embryogenesis, wound healing and carcinoma pathogenesis to drive epithelial cells towards a mesenchymal state. During carcinoma progression, EMT enables the cells forming these tumours to acquire the traits of highly malignant cells, notably motility, invasiveness and an ability to disseminate to form distant metastases. Indeed, a number of published reports have associated EMT with a variety of malignant carcinoma cells. Recently, however, Zheng et al.1 reported that in genetically engineered mouse models of pancreatic adenocarcinoma development, carcinoma cells could metastasize without activating EMT programs. Their conclusions, if sustained by the evidence presented, would prompt a major change in how we conceptualize malignant progression and metastasis of carcinoma cells, including the neoplastic cells in human carcinomas.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1: αSMA is an unreliable marker of EMT in the KPCY model of pancreatic cancer.

References

  1. Zheng, X. et al. Epithelial-to-mesenchymal transition is dispensable for metastasis but induces chemoresistance in pancreatic cancer. Nature 527, 525–530 (2015)

    Article  ADS  CAS  Google Scholar 

  2. Rhim, A. D. et al. EMT and dissemination precede pancreatic tumor formation. Cell 148, 349–361 (2012)

    Article  CAS  Google Scholar 

  3. Nieto, M. A., Huang, R. Y., Jackson, R. A. & Thiery, J. P. EMT: 2016. Cell 166, 21–45 (2016)

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Departments of Medicine and Cell and Developmental Biology, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, 19104, Pennsylvania, USA

    Nicole M. Aiello & Ben Z. Stanger

  2. Experimental Medicine I, Nikolaus-Fiebiger-Center for Molecular Medicine, FAU University of Erlangen-Nuernberg, Erlangen, 91054, Germany

    Thomas Brabletz

  3. Department of Molecular Biology, Princeton University, Princeton, 08544, New Jersey, USA

    Yibin Kang

  4. Instituto de Neurociencias CSIC-UMH, Avda. Ramón y Cajal s/n, San Juan de Alicante, 03550, Spain

    M. Angela Nieto

  5. Whitehead Institute for Biomedical Research, Cambridge, 02142, Massachusetts, USA

    Robert A. Weinberg

  6. Ludwig/MIT Center for Molecular Oncology, Cambridge, 02142, Massachusetts, USA

    Robert A. Weinberg

  7. Department of Biology, Massachusetts Institute of Technology, Cambridge, 02142, Massachusetts, USA

    Robert A. Weinberg

Authors
  1. Nicole M. Aiello
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Thomas Brabletz
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Yibin Kang
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. M. Angela Nieto
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Robert A. Weinberg
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Ben Z. Stanger
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

N.M.A. produced and analysed the experimental data; T.B., Y.K., M.A.N., R.A.W. and B.Z.S. conceived and wrote the manuscript.

Corresponding author

Correspondence to Ben Z. Stanger.

Ethics declarations

Competing interests

R.A.W. is listed as an inventor on three patent applications filed by the Whitehead Institute for Biomedical Research relating to the formation of cancer stem cells through activation of an EMT program. US patent application number US 14/441,697 describes a method to use PKC-α/FRA1 pathway inhibitors to target carcinoma cells that are identified by their increased expression of EMT-related genes. US patent application number US 15/307,657 describes a method to induce cancer stem cells to undergo EMT, rendering them amenable to conventional treatments. US patent application number US 14/065,311 describes methods for identifying compounds and compositions that target cancer stem cells, including cancer stem cells that have undergone EMT. R.A.W. is also listed as an inventor on two related patents that have been granted. US patent number US9212347 describes methods for preparing progenitor cells by inducing EMT. US patent number US9308238 describes methods and compounds for modulating and inducing EMT. R.A.W. is also a cofounder of Verastem Inc.

PowerPoint slides

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Aiello, N., Brabletz, T., Kang, Y. et al. Upholding a role for EMT in pancreatic cancer metastasis. Nature 547, E7–E8 (2017). https://doi.org/10.1038/nature22963

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nature22963

This article is cited by

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.

Search

Advanced search

Quick links

Nature Briefing: Cancer

Sign up for the Nature Briefing: Cancer newsletter — what matters in cancer research, free to your inbox weekly.

Get what matters in cancer research, free to your inbox weekly. Sign up for Nature Briefing: Cancer