Fischer et al. reply (original) (raw)

Nature volume 547, pages E5–E6 (2017)Cite this article

Subjects

Replying to X. Ye et al. Nature 547, 10.1038/nature22816 (2017)

In our original paper, we demonstrated, using a novel lineage tracing reporter system, that the epithelial-to-mesenchymal transition (EMT) is not necessary for metastasis but contributes to chemoresistance1. In the accompanying Comment[2](/articles/nature22817#ref-CR2 "Ye, X. et al. Upholding a role for EMT in pancreatic cancer metastasis. Nature 547, http://dx.doi.org/10.1038/nature22817

             (2017)"), Ye _et al_. begin by advocating for hypothetical definitions of EMT[3](/articles/nature22817#ref-CR3 "Nieto, M. A., Huang, R. Y., Jackson, R. A. & Thiery, J. P. EMT: 2016. Cell 166, 21–45 (2016)"), including concepts such as “various versions of EMT”, “certain versions of EMT” and “partial” EMT. In our view, these concepts are not well-defined by molecular characterization, nor is there direct evidence of their requirement in metastasis; thus we disagree that they can be used to interpret our findings. Ye _et al._[2](/articles/nature22817#ref-CR2 "Ye, X. et al. Upholding a role for EMT in pancreatic cancer metastasis. Nature 547, 
              http://dx.doi.org/10.1038/nature22817
              
             (2017)") also suggest that Fsp1–Cre or Vim–CreER are inadequate in reporting EMT, and that miR-200 overexpression may not have inhibited EMT. Here, we wish to provide clarity regarding the tools we have used in our study.

References

  1. Fischer, K. R. et al. Epithelial-to-mesenchymal transition is not required for lung metastasis but contributes to chemoresistance. Nature 527, 472–476 (2015)
    Article ADS CAS PubMed PubMed Central Google Scholar
  2. Ye, X. et al. Upholding a role for EMT in pancreatic cancer metastasis. Nature 547, http://dx.doi.org/10.1038/nature22817 (2017)
  3. Nieto, M. A., Huang, R. Y., Jackson, R. A. & Thiery, J. P. EMT: 2016. Cell 166, 21–45 (2016)
    Article CAS Google Scholar
  4. Kalluri, R. & Weinberg, R. A. The basics of epithelial-mesenchymal transition. J. Clin. Invest. 119, 1420–1428 (2009)
    Article CAS PubMed PubMed Central Google Scholar
  5. Rhim, A. D. et al. EMT and dissemination precede pancreatic tumor formation. Cell 148, 349–361 (2012)
    Article CAS PubMed PubMed Central Google Scholar
  6. Ye, X. et al. Distinct EMT programs control normal mammary stem cells and tumour-initiating cells. Nature 525, 256–260 (2015)
    Article ADS CAS PubMed PubMed Central Google Scholar
  7. Tran, H. D. et al. Transient SNAIL1 expression is necessary for metastatic competence in breast cancer. Cancer Res. 74, 6330–6340 (2014)
    Article CAS PubMed PubMed Central Google Scholar
  8. Ni, T. et al. Snail1-dependent p53 repression regulates expansion and activity of tumour-initiating cells in breast cancer. Nat. Cell Biol. 18, 1221–1232 (2016)
    Article CAS PubMed PubMed Central Google Scholar
  9. 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 PubMed PubMed Central Google Scholar
  10. Korpal, M. et al. Direct targeting of Sec23a by miR-200s influences cancer cell secretome and promotes metastatic colonization. Nat. Med. 17, 1101–1108 (2011)
    Article CAS PubMed PubMed Central Google Scholar
  11. Cheung, K. J. et al. Polyclonal breast cancer metastases arise from collective dissemination of keratin 14-expressing tumor cell clusters. Proc. Natl Acad. Sci. USA 113, E854–E863 (2016)
    CAS PubMed PubMed Central Google Scholar
  12. Cheung, K. J., Gabrielson, E., Werb, Z. & Ewald, A. J. Collective invasion in breast cancer requires a conserved basal epithelial program. Cell 155, 1639–1651 (2013)
    Article CAS PubMed PubMed Central Google Scholar

Download references

Author information

Authors and Affiliations

  1. Department of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, 10065, New York, USA
    Kari R. Fischer, Nasser K. Altorki, Vivek Mittal & Dingcheng Gao
  2. Department of Cell and Developmental Biology, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, 10065, New York, USA
    Kari R. Fischer, Vivek Mittal & Dingcheng Gao
  3. Neuberger Berman Lung Cancer Center, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, 10065, New York, USA
    Kari R. Fischer, Nasser K. Altorki, Vivek Mittal & Dingcheng Gao
  4. Weill Cornell Graduate School of Medical Sciences, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, 10065, New York, USA
    Kari R. Fischer
  5. The New York Academy of Science, 250 Greenwich St, New York, 10007, New York, USA
    Kari R. Fischer

Authors

  1. Kari R. Fischer
  2. Nasser K. Altorki
  3. Vivek Mittal
  4. Dingcheng Gao

Corresponding author

Correspondence toDingcheng Gao.

PowerPoint slides

Rights and permissions

About this article

Cite this article

Fischer, K., Altorki, N., Mittal, V. et al. Fischer et al. reply.Nature 547, E5–E6 (2017). https://doi.org/10.1038/nature22817

Download citation

This article is cited by