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.

  • NEWS AND VIEWS

Fatty acids prime the lung as a site for tumour spread

The mechanisms that enable the deadly spread of cancer are not fully understood. It emerges that tumours can signal to the lung to manipulate lipids and so prime the organ to support tumour cells that subsequently spread there.
  1. Laura V. Pinheiro

    1. Laura V. Pinheiro is in the Department of Cancer Biology and at the Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.

    View author publications

    You can also search for this author in PubMed  Google Scholar

  2. Kathryn E. Wellen

    1. Kathryn E. Wellen is in the Department of Cancer Biology and at the Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.

    View author publications

    You can also search for this author in PubMed  Google Scholar

Cancer cells require nutrients such as glucose, amino acids and fatty acids to grow and proliferate. They also require nutrients to disperse and grow in organs distant from the initial (primary) tumour site — a spreading process called metastasis. The nutritional environment affects whether cancer cells can thrive in a new location. Tumour cells are known to secrete factors that act on distant sites ahead of their arrival, to prepare a favourable environment, termed a pre-metastatic niche1. However, nutritional aspects of the pre-metastatic niche are poorly understood. Writing in Nature Cancer, Altea-Manzano et al.2 reveal how breast cancer cells program the metabolic environment in the lung before colonization, to support metastatic growth.

Access options

Rent or buy this article

Get just this article for as long as you need it

$39.95

Learn more

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

Nature 615, 224-225 (2023)

doi: https://doi.org/10.1038/d41586-023-00538-8

References

  1. Peinado, H. et al. Nature Rev. Cancer 17, 302–317 (2017).

    Article  PubMed  Google Scholar 

  2. Altea-Manzano, P. et al. Nature Cancer https://doi.org/10.1038/s43018-023-00513-2 (2023).

    Article  Google Scholar 

  3. Broadfield, L. A., Pane, A. A., Talebi, A., Swinnen, J. V. & Fendt. S.-M. Dev. Cell 56, 1363–1393 (2021).

    Article  PubMed  Google Scholar 

  4. Martin-Perez, M., Urdiroz-Urricelqui, U., Bigas, C. & Benitah, S. A. Cell Metab. 34, 1675–1699 (2022).

    Article  PubMed  Google Scholar 

  5. Elia, I. et al. Nature 568, 117–121 (2019).

    Article  PubMed  Google Scholar 

  6. Sivanand, S., Viney, I. & Wellen, K. E. Trends Biochem. Sci. 43, 61–74 (2018).

    Article  PubMed  Google Scholar 

  7. Agudelo, C. W., Samaha, G. & Garcia-Arcos, I. Lipids Health Dis. 19, 122 (2020).

    Article  PubMed  Google Scholar 

  8. Pascual, G. et al. Nature 599, 485–490 (2021).

    Article  PubMed  Google Scholar 

  9. Ferraro, G. B. et al. Nature Cancer 2, 414–428 (2021).

    Article  PubMed  Google Scholar 

  10. Batchuluun, B., Pinkosky, S. L. & Steinberg, G. R. Nature Rev. Drug Discov. 21, 283–305 (2022).

    Article  PubMed  Google Scholar 

Download references

Competing Interests

The authors declare no competing interests.

Subjects

Latest on:

Nature Careers

Jobs

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing

Search

Advanced search

Quick links