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10.1038/srep24728

http://scihub22266oqcxt.onion/10.1038/srep24728
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C4835760!4835760!27090737
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suck abstract from ncbi


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pmid27090737      Sci+Rep 2016 ; 6 (ä): ä
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  • Knockdown of lncRNA-ATB suppresses autocrine secretion of TGF-?2 by targeting ZNF217 via miR-200c in keloid fibroblasts #MMPMID27090737
  • Zhu HY; Bai WD; Li C; Zheng Z; Guan H; Liu JQ; Yang XK; Han SC; Gao JX; Wang HT; Hu DH
  • Sci Rep 2016[]; 6 (ä): ä PMID27090737show ga
  • Abnormally high activation of transforming growth factor-? (TGF-?) signaling has been demonstrated to be involved in the initiation and progression of keloids. However, the functional role of long non-coding RNA (lncRNA)-activated by TGF-? (lncRNA-ATB) in keloids has not been documented. Here we investigated the role of lncRNA-ATB in the autocrine secretion of TGF-? in keloid fibroblasts (KFs) and explored the underlying molecular mechanism. Using immunohistochemistry and quantitative RT-PCR analysis, we showed that lncRNA-ATB and ZNF217, a transcriptional activator of TGF-?, were overexpressed and miR-200c, which targets ZNF217, was under-expressed in keloid tissue and keloid fibroblasts. Through gain- and loss-of-function studies, we demonstrated that knockdown of lncRNA-ATB decreased autocrine secretion of TGF-?2 and ZNF217 expression but upregulated expression of miR-200c in KFs. Stable downregulation of ZNF217 expression decreased the autocrine secretion of TGF-?2. miR-200c was endogenously associated with lncRNA-ATB, and inhibition of miR-200c overcame the decrease in ZNF217 expression in KFs. Taken together, these findings indicate that lncRNA-ATB governs the autocrine secretion of TGF-?2 in KFs, at least in part, by downregulating the expression level of ZNF217 via miR-200c, suggesting a signaling axis consisting of lncRNA-ATB/miR-200c/ZNF217/TGF-?2. These findings may provide potential biomarkers and targets for novel diagnostic and therapeutic approaches for keloids.
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