Abstract:
:Alu sequences are the most abundant short interspersed repeated elements in the human genome. Here we show that in a cell culture model of colorectal cancer (CRC) progression, we observe accumulation of Alu RNA that is associated with reduced DICER1 levels. Alu RNA induces epithelial-to-mesenchymal transition (EMT) by acting as a molecular sponge of miR-566. Moreover, Alu RNA accumulates as consequence of DICER1 deficit in colorectal, ovarian, renal and breast cancer cell lines. Interestingly, Alu RNA knockdown prevents DICER1 depletion-induced EMT despite global microRNA (miRNA) downregulation. Alu RNA expression is also induced by transforming growth factor-β1, a major driver of EMT. Corroborating this data, we found that non-coding Alu RNA significantly correlates with tumor progression in human CRC patients. Together, these findings reveal an unexpected DICER1-dependent, miRNA-independent role of Alu RNA in cancer progression that could bring mobile element transcripts in the fields of cancer therapeutic and prognosis.
journal_name
Oncogenejournal_title
Oncogeneauthors
Di Ruocco F,Basso V,Rivoire M,Mehlen P,Ambati J,De Falco S,Tarallo Vdoi
10.1038/onc.2017.369subject
Has Abstractpub_date
2018-02-01 00:00:00pages
627-637issue
5eissn
0950-9232issn
1476-5594pii
onc2017369journal_volume
37pub_type
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