Tumor metastasis to lymph nodes requires YAP-dependent metabolic adaptation

Author:

Lee Choong-kun1ORCID,Jeong Seung-hwan12,Jang Cholsoon3ORCID,Bae Hosung12ORCID,Kim Yoo Hyung12,Park Intae12,Kim Sang Kyum4ORCID,Koh Gou Young12ORCID

Affiliation:

1. Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.

2. Center for Vascular Research, Institute for Basic Science (IBS), Daejeon 34141, Republic of Korea.

3. Lewis Sigler Institute for Integrative Genomics and Department of Chemistry, Princeton University, Washington Road, Princeton, NJ 08544, USA.

4. Department of Pathology, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.

Abstract

Fueling lymph node metastases Metastatic cells can migrate from a primary tumor to distant organs through two routes: They can enter the bloodstream directly, or they can enter a lymph node adjacent to the primary tumor. Little is known about the biological mechanisms that allow tumor cells to survive and grow within lymph nodes. Studying mouse models, Lee et al. found that tumor cells adapt to the lymph node microenvironment by shifting their metabolism toward fatty acid oxidation. This occurs through activation of a signaling pathway driven by the yes-associated protein (YAP) transcription factor. Importantly, inhibition of fatty acid oxidation or YAP signaling suppressed lymph node metastasis in the mice. Science , this issue p. 644

Funder

Institute for Basic Science

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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