Genetic Analysis Reveals AMPK Is Required to Support Tumor Growth in Murine Kras-Dependent Lung Cancer Models

Lillian J. Eichner; Sonja N. Brun; Sébastien Herzig; Nathan P. Young; Stephanie D. Curtis; David B. Shackelford; Maxim N. Shokhirev; Mathias Leblanc; Liliana I. Vera; Amanda Hutchins; Debbie S. Ross; Reuben J. Shaw; Robert U. Svensson

doi:10.1016/j.cmet.2018.10.005

Genetic Analysis Reveals AMPK Is Required to Support Tumor Growth in Murine Kras-Dependent Lung Cancer Models

Lillian J. Eichner, Sonja N. Brun, Sébastien Herzig, Nathan P. Young, Stephanie D. Curtis, David B. Shackelford, Maxim N. Shokhirev, Mathias Leblanc, Liliana I. Vera, Amanda Hutchins, Debbie S. Ross, Reuben J. Shaw^*, Robert U. Svensson

^*Corresponding author for this work

Biochemistry and Molecular Genetics

Research output: Contribution to journal › Article › peer-review

145 Scopus citations

Abstract

AMPK can either inhibit or promote tumor growth depending on tumor type and context. Eichner et al. show that AMPK, unlike LKB1, has a pro-tumorigenic role in a Kras-dependent, non-small-cell lung cancer model through the regulation of Tfe3, a master regulator of lysosomes, which supports lung tumor growth.

Original language	English (US)
Pages (from-to)	285-302.e7
Journal	Cell Metabolism
Volume	29
Issue number	2
DOIs	https://doi.org/10.1016/j.cmet.2018.10.005
State	Published - Feb 5 2019

Funding

This study was supported by grants to R.J.S. from the National Institutes of Health ( R35CA220538 , P01CA120964 ) and the Samuel Waxman Cancer Research Foundation and by The Leona M. and Harry B. Helmsley Charitable Trust grant # 2012-PG-MED002 . R.U.S. is supported by a postdoctoral fellowship from the American Cancer Society (ACS# 124183-PF-13-023-01-CSM ). L.J.E. is supported by a postdoctoral fellowship from the American Cancer Society ( PF-15-037-01-DMC ). S.N.B was supported by training grant 5T32CA009370 to the Salk Institute Cancer Center and 5F32CA206400 . The Salk CCSG P30 CA014195 and Helmsley Charitable Trust supported the Functional Genomics Core and the Bioinformatics Core, as well as providing partial support for K. McIntyre and the histology core of the Salk Institute.

Keywords

AMPK
Kras
LKB1
Tfe3
Tfeb
cancer
lung
lysosomes
metabolism
tumor

ASJC Scopus subject areas

Physiology
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.cmet.2018.10.005

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Eichner, L. J., Brun, S. N., Herzig, S., Young, N. P., Curtis, S. D., Shackelford, D. B., Shokhirev, M. N., Leblanc, M., Vera, L. I., Hutchins, A., Ross, D. S., Shaw, R. J., & Svensson, R. U. (2019). Genetic Analysis Reveals AMPK Is Required to Support Tumor Growth in Murine Kras-Dependent Lung Cancer Models. Cell Metabolism, 29(2), 285-302.e7. https://doi.org/10.1016/j.cmet.2018.10.005

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abstract = "AMPK can either inhibit or promote tumor growth depending on tumor type and context. Eichner et al. show that AMPK, unlike LKB1, has a pro-tumorigenic role in a Kras-dependent, non-small-cell lung cancer model through the regulation of Tfe3, a master regulator of lysosomes, which supports lung tumor growth.",

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Genetic Analysis Reveals AMPK Is Required to Support Tumor Growth in Murine Kras-Dependent Lung Cancer Models

Abstract

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

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