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• W2306562666 abstract "Long non-coding RNAs (lncRNAs) have emerged as critical regulators in various cellular processes. However, the potential involvement of lncRNAs in kinase signalling remains largely unknown. AMP-activated protein kinase (AMPK) acts as a critical sensor of cellular energy status. Here we show that the lncRNA NBR2 (neighbour of BRCA1 gene 2) is induced by the LKB1–AMPK pathway under energy stress. On energy stress, NBR2 in turn interacts with AMPK and promotes AMPK kinase activity, thus forming a feed-forward loop to potentiate AMPK activation during energy stress. Depletion of NBR2 attenuates energy-stress-induced AMPK activation, resulting in unchecked cell cycling, altered apoptosis/autophagy response, and increased tumour development in vivo. NBR2 is downregulated and its low expression correlates with poor clinical outcomes in some human cancers. Together, the results of our study uncover a mechanism coupling lncRNAs with metabolic stress response, and provides a broad framework to understand further the regulation of kinase signalling by lncRNAs. Liu et al. show that, in response to energy stress, the NBR2 long non-coding RNA binds AMPK and promotes its activity to reduce cancer cell proliferation. Conversely, loss of NBR2 inhibits AMPK, leading to mTOR activation and tumour growth." @default.
• W2306562666 created "2016-06-24" @default.
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• W2306562666 date "2016-03-21" @default.
• W2306562666 modified "2023-10-05" @default.
• W2306562666 title "LncRNA NBR2 engages a metabolic checkpoint by regulating AMPK under energy stress" @default.
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• W2306562666 doi "https://doi.org/10.1038/ncb3328" @default.
• W2306562666 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4814347" @default.
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