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


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-10-04

AUTHORS

Zhen-Dong Xiao, Leng Han, Hyemin Lee, Li Zhuang, Yilei Zhang, Joelle Baddour, Deepak Nagrath, Christopher G. Wood, Jian Gu, Xifeng Wu, Han Liang, Boyi Gan

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. More... »

PAGES

783

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  • Journal

    TITLE

    Nature Communications

    ISSUE

    1

    VOLUME

    8

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-017-00902-z

    DOI

    http://dx.doi.org/10.1038/s41467-017-00902-z

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1092023282

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28978906


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