Journal
ADVANCED SCIENCE
Volume 7, Issue 4, Pages -Publisher
WILEY
DOI: 10.1002/advs.201900949
Keywords
circular RNA; hepatocellular cancer stem cells; miR-6887-3p; PAX5; ribosomes; self-renewal
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Funding
- State Key Program of National Natural Science Foundation of China [81730076]
- China National Funds for Distinguished Young Scientists [81425019]
- Shanghai Science and Technology Committee Program [18XD1405300]
- State Key Laboratory of Oncogenes and Related Genes [90-17-04]
- National Institutes of Health [EB021339]
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Both circular RNAs (circRNAs) and cancer stem cells (CSCs) are separately known to be involved in cancer, but their interaction remains unclear. Here, the regulation of hepatocellular CSC self-renewal is discovered by a circRNA, circ-MALAT1, which is produced by back-splicing of a long noncoding RNA, MALAT1. Circ-MALAT1 is highly expressed in CSCs from clinical hepatocellular carcinoma samples under the mediation of an RNA-binding protein, AUF1. Surprisingly, circMALAT1 functions as a brake in ribosomes to retard PAX5 mRNA translation and promote CSCs' self-renewal by forming an unprecedented ternary complex with both ribosomes and mRNA. The discovered braking mechanism of a circRNA, termed mRNA braking, along with its more traditional role of miRNA sponging, uncovers a dual-faceted pattern of circRNA-mediated post-transcriptional regulation for maintaining a specific cell state.
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