The aim of the present study was to investigate whether class c1 decoy oligodeoxynucleotides (odns) can inhibit the expression of pro-fibrotic genes associated with rat hepatic stellate cell (HSC) activation and hepatic fibrosis. luciferase reporter assays were performed to test the promoter activities of transforming growth factor (TGF)-β and its downstream target genes following transfection of decoy odns and plasmids into HSc-T6 cells, and western blot assays were performed to measure the protein expression of those genes following decoy ODN transfection. Class C1 decoy ODNs were confirmed to inhibit the promoter activity of TGF-β and its downstream target genes, such as type 1 collagen (coli)α1, tissue inhibitor of metalloproteinases (TiMP)1 and α-smooth muscle actin by Gaussia luciferase reporter assay, and to further downregulate the expression of TGF-β, SMad3, coliα1 and TiMP1 by western blotting in activated HSC-T6 cells. In conclusion, class C1 decoy ODNs inhibited pro-fibrotic gene expression in rat HSCS by downregulating TGF-β signaling.

OCT4 is a major transcription factor that maintains the pluripotency of stem cells, including embryonic stem cells, induced pluripotent stem cells and cancer stem cells. An increasing number of long noncoding RNAs have been reported to participate in the regulation of OCT4 expression through various mechanisms, including binding with the OCT4 gene promoter to regulate local methylation; promoting chromosomal spatial folding to form an inner ring, thereby aggregating OCT4 cis-acting elements scattered in discontinuous sites of the chromosome; competitively binding microRNAs with OCT4 to upregulate OCT4 expression at the posttranscriptional level; and sharing a promoter with OCT4. Moreover, the transcription of some long noncoding RNAs is regulated by OCT4, and certain long noncoding RNAs form feedback regulatory loops with OCT4. In this review, we summarized the research progress of the long noncoding RNAs involved in the regulation of OCT4 expression.

No abstract