Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-017-00902-z
Keywords
-
Categories
Funding
- MD Anderson Cancer Center, Cancer Prevention & Research Institute of Texas [RP130020]
- National Institutes of Health [CA181196, CA190370, CA143883, CA175486, CA016672]
- Ellison Medical Foundation [AG-NS-0973-13]
- Gabrielle's Angel Foundation for Cancer Research
- R. Lee Clark Fellow Award from Jeanne F. Shelby Scholarship Fund
- Cancer Prevention and Research Institute of Texas [RP140462]
- Mary K. Chapman Foundation
- Lorraine Dell Program in Bioinformatics for Personalization of Cancer Medicine
Ask authors/readers for more resources
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 noncoding 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available