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BMC Proceedings

Volume 6 Supplement 3

Metabolism, diet and disease

Open Access

Altered metabolic requirements in cancer cell migration and metastasis

  • Jaewon Lee1, 2,
  • M Rosa Ng1,
  • Kerstin W Sinkevicius3, 4, 5,
  • Carla F Kim3, 4, 5,
  • Gaudenz Danuser1,
  • Joan S Brugge1 and
  • Marcia C Haigis1, 2
BMC Proceedings20126(Suppl 3):P32

Published: 1 June 2012


Metastasis poses a great challenge in clinical management of many cancers. Metabolic demands of cancer cell proliferation – i.e. elevated aerobic glycolysis for biomass generation – have been well characterized, but the contribution of altered metabolism to metastasis remains to be elucidated. While elevated aerobic glycolysis, a phenomenon termed Warburg effect, is a hallmark of proliferative tumor cells, emerging evidence suggests that metastatic cancer cells have an opposite phenotype.

Materials and methods

We investigated the metabolism in cell lines of different metastatic capacity. In addition, to quantitatively study cell migration and metabolism, we used MCF10A breast epithelial cells with fluorescent histone tags along with live cell imaging and tracking by a custom MATLAB program to measure speed and behavior of migration.


Our preliminary data suggest that the more metastatic cancer cells depend on mitochondrial metabolism. Furthermore, changing mitochondrial metabolism in MCF10A breast epithelial cell line affected not only the speed but also the pattern of cell migration. Consistent with the altered migratory behaviors, stimulation of mitochondrial metabolism changed cell adhesion markers.


In sum, we show evidence that mitochondrial metabolism plays an important role in promoting cell migration and altering cell adhesion with implications for cancer metastasis.

Authors’ Affiliations

Department of Cell Biology, Harvard Medical School
The Paul F. Glenn Labs for the Biological Mechanisms of Aging, Harvard Medical School
Stem Cell Program, Children’s Hospital Boston
Department of Genetics, Harvard Medical School
Harvard Stem Cell Institute


© Lee et al; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.