Loss of AMPKα2 promotes melanoma tumor growth and brain metastasis

Ping Yuan, Da Teng, Evelyn de Groot, Man Li, Sebastian Trousil, Che Hung Shen, Jason Roszik, Michael A. Davies, Y. N.Vashisht Gopal, Bin Zheng

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

AMP-activated protein kinase (AMPK) is a critical cellular energy sensor at the interface of metabolism and cancer. However, the role of AMPK in carcinogenesis remains unclear. Here, through analysis of the TCGA melanoma dataset, we found that PRKAA2 gene that encodes the α2 subunit of AMPK is mutated in ∼9% of cutaneous melanomas, and these mutations tend to co-occur with NF1 mutations. Knockout of AMPKα2 promoted anchorage-independent growth of NF1-mutant melanoma cells, whereas ectopic expression of AMPKα2 inhibited their growth in soft agar assays. Moreover, loss of AMPKα2 accelerated tumor growth of NF1-mutant melanoma and enhanced their brain metastasis in immune-deficient mice. Our findings support that AMPKα2 serves as a tumor suppressor in NF1-mutant melanoma and suggest that AMPK could be a therapeutic target for treating melanoma brain metastasis.

Original languageEnglish (US)
Article number106791
JournaliScience
Volume26
Issue number6
DOIs
StatePublished - Jun 16 2023

Keywords

  • Biological database
  • Cancer
  • Molecular Genetics

ASJC Scopus subject areas

  • General

Fingerprint

Dive into the research topics of 'Loss of AMPKα2 promotes melanoma tumor growth and brain metastasis'. Together they form a unique fingerprint.

Cite this