>Ctnnb1|NM_001165902|3'UTR
   1 ATCGTCCTTTAGGTAAGAAAGCTTATAAAAGCCAGTGTGGGTGAATACTTTACTCTGCCTGCAGAACTCCAGAAAGACTT
  81 GGTAGGGTGGGAATGGTTTTAGGCCTGTTTGTAAATCTGCCACCAAACAGATACATACCTTGGAAGGAGATGTTCATGTG
 161 TGGAAGTTTCTCACGTTGATGTTTTTGCCACAGCTTTTGCAGCGTTATACTCAGATGAGTAACATTTGCTGTTTTCAACA
 241 TTAATAGCAGCCTTTCTCTCTATACAGCTGTAGTGTCTGAACGTGCATTGTGATTGGCCTGTAGAGTTGCTGAGAGGGCT
 321 CGAGGGGTGGGCTGGTATCTCAGAAAGTGCCTGACACACTAACCAAGCTGAGTTTCCTATGGGAACAGTCGAAGTACGCT
 401 TTTTGTTCTGGTCCTTTTTGGTCGAGGAGTAACAATACAAATGGATTTGGGGAGTGACTCACGCAGTGAAGAATGCACAC
 481 GAATGGATCACAAGATGGCGTTATCAAACCCTAGCCTTGCTTGTTCTTTGTTTTAATATCTGTAGTGGTGCTGACTTTGC
 561 TTGCTTTTATTTTTTGCAGTAACTGTTAGTTTTTAAGTAGTGTTATGTTCTAGTGAACCTGCTACAGCAATTTCTGATTT
 641 CTAAGAACCGAGTAATGGTGTAGAACACTAATTCATAATCACGCTAATTGTAATCTGGAGACGTGTAACATTGTGTAGCC
 721 TTTTGTATAAATAGACAGATAGAAATGGTCCGATTAGTTTCCTTTTTAATATGCTTAAAATAAGCAGGTGGATCTATTTC
 801 ATGTTTTTGAACAAAAACTTTATCGGGGATACGTGCGGTAGGGTAAATCAGTAAGAGGTGTTATTTGAGCCTTGTTTTGG
 881 ACAGTATACCAGTTGCCTTTTATCCCAAAGTTGTTGTAACCTGCTGTGATACAATGCTTCAACAGATGCGGTTATAGAAA
 961 TGGTTCAGAATTAAACTTTTAATTCATTCAAAAAAAAAAAAAAAAAA

ID	Duplex structure	Position	Score	MFE
1	miRNA 3' aaacCAACA--CUCGGAUCGGAAa 5' ||| | | ||||||||| Target 5' tggcGTTATCAAACCCTAGCCTTg 3'	496 - 519	156.00	-13.20
2	miRNA 3' aaaccAACACUCGGAUCGGAAa 5' ||||| ||||||| Target 5' taacaTTGTG----TAGCCTTt 3'	706 - 723	151.00	-11.50
3	miRNA 3' aaacCAACACUCGGAUCGGAAa 5' | ||| | :: |||||| Target 5' aagaGGTGTTATTTGAGCCTTg 3'	853 - 874	126.00	-11.29

- Biochimica et biophysica acta, 2014

Versican is an extracellular chondroitin sulfate proteoglycan which functions as a structural molecule but can also regulate a variety of cellular activities. This study was designed to explore the roles of versican in the process of dermal wound repair. To elevate levels of versican, we ectopically expressed the versican 3'-untranslated region (3'UTR) as a competitive endogenous RNA to modulate expression of versican. We demonstrated that wounds closed faster in transgenic mice expressing the versican 3'UTR, as compared to those in wildtype mice. We stably expressed versican 3'UTR in NIH3T3 fibroblasts and found that the 3'UTR-transfected cells showed increased migratory capacity relative to vector-transfected cells. Interestingly, we found that the 3'UTRs of versican and beta-catenin shared common microRNAs (miRNAs) including miR-185, miR-203*, miR-690, miR-680, and miR-434-3p. Luciferase assays showed that all of these miRNAs could target the 3'UTRs of both versican and beta-catenin, when the luciferase constructs contained fragments harboring the miRNA binding sites. As a consequence, expression of both versican and beta-catenin was up-regulated, which was confirmed in vitro and in vivo. Transfection with small interfering RNAs (siRNAs) targeting the versican 3'UTR abolished the 3'UTR's effects on cell migration and invasion. Taken together, these results demonstrate that versican plays important roles in wound repair and that versican messenger RNAs (mRNAs) could compete with endogenous RNAs for regulating miRNA functions.