Journal
CELLULAR MICROBIOLOGY
Volume 21, Issue 9, Pages -Publisher
WILEY
DOI: 10.1111/cmi.13043
Keywords
apoptosis; EV71; GADD45 beta; lncRNA; miRNA
Categories
Funding
- EID [MOST104-2321-B-002-047, MOST105-2321-B-002-012, MOST106-2321-B-002-004] Funding Source: Medline
- NRPB [MOST105-2325-B-002-002, MOST103-2325-B-002-035, MOST104-2325-B-002-008] Funding Source: Medline
- MOST [MOST105-2320-B-002-066] Funding Source: Medline
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Enterovirus 71 (EV71) is an emerging life-threatening pathogen particularly in the Asia-Pacific region. Apoptosis is a major pathogenic feature in EV71 infection. However, which molecular mechanism participating in EV71-induced apoptosis is not completely understood. Long noncoding RNAs (lncRNAs), a newly discovered class of regulatory RNA molecules, govern a wide range of biological functions through multiple regulatory mechanisms. Whether lncRNAs involved in EV71-induced apoptosis was investigated in this study. We conducted an apoptosis-oriented approach by integrating lncRNA and mRNA profilings. lnc-IRAK3-3 is down-regulated in EV71 infection and plays an important role in EV71 infection-induced apoptosis. Compensation of lnc-IRAK3-3 in EV71 infection promoted cell apoptosis wherein GADD45 beta expression was increased and further triggered caspase3 and PARP cleavage. Using bioinformatics analysis and functional assays, lnc-IRAK3-3 could functionally sequester miR-891b and GADD45 beta 3 ' UTR whereas miR-891b showed the inhibitory activity on GADD45 beta expression. Taken together, lnc-IRAK3-3 has the ability capturing miR-891b to enforce GADD45 beta expression and eventually promotes apoptosis. On the contrary, host cells suppress lnc-IRAK3-3 to relieve lnc-IRAK3-3-sequestered miR-891b, restrain GADD45 beta, and attenuate apoptosis in EV71 infection that prevent host cells from severe damages. We discover a new molecular mechanism by which host cells counteract EV71-induced apoptosis through the lnc-IRAK3-3/miR-891b/GADD45 beta axis partially.
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