Energy stress-induced lncRNA FILNC1 represses c-Myc-mediated energy metabolism and inhibits renal tumor development

Zhen-Dong Xiao, Leng Han, Hyemin Lee, Li Zhuang, Yilei Zhang, Joelle Baddour, Deepak Nagrath, Christopher G. Wood, Jian Gu, Xifeng Wu, Han Liang and Boyi Gan ()
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Zhen-Dong Xiao: The University of Texas MD Anderson Cancer Center
Leng Han: The University of Texas MD Anderson Cancer Center
Hyemin Lee: The University of Texas MD Anderson Cancer Center
Li Zhuang: The University of Texas MD Anderson Cancer Center
Yilei Zhang: The University of Texas MD Anderson Cancer Center
Joelle Baddour: Rice University
Deepak Nagrath: University of Michigan
Christopher G. Wood: The University of Texas MD Anderson Cancer Center
Jian Gu: The University of Texas MD Anderson Cancer Center
Xifeng Wu: The University of Texas MD Anderson Cancer Center
Han Liang: The University of Texas MD Anderson Cancer Center
Boyi Gan: The University of Texas MD Anderson Cancer Center

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract The roles of long non-coding RNAs in cancer metabolism remain largely unexplored. Here we identify FILNC1 (FoxO-induced long non-coding RNA 1) as an energy stress-induced long non-coding RNA by FoxO transcription factors. FILNC1 deficiency in renal cancer cells alleviates energy stress-induced apoptosis and markedly promotes renal tumor development. We show that FILNC1 deficiency leads to enhanced glucose uptake and lactate production through upregulation of c-Myc. Upon energy stress, FILNC1 interacts with AUF1, a c-Myc mRNA-binding protein, and sequesters AUF1 from binding c-Myc mRNA, leading to downregulation of c-Myc protein. FILNC1 is specifically expressed in kidney, and is downregulated in renal cell carcinoma; also, its low expression correlates with poor clinical outcomes in renal cell carcinoma. Together, our study not only identifies FILNC1 as a negative regulator of renal cancer with potential clinical value, but also reveals a regulatory mechanism by long non-coding RNAs to control energy metabolism and tumor development.

Date: 2017
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DOI: 10.1038/s41467-017-00902-z

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