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Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Mol+Med+(Berl) 2018 ; 96 (3): 301-13 Nephropedia Template TP
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TGF-?-induced NKILA inhibits ESCC cell migration and invasion through NF-?B/MMP14 signaling #MMPMID29379981
Lu Z; Chen Z; Li Y; Wang J; Zhang Z; Che Y; Huang J; Sun S; Mao S; Lei Y; Gao Y; He J
J Mol Med (Berl) 2018[]; 96 (3): 301-13 PMID29379981show ga
Abstract: The transforming growth factor ? (TGF-?) signaling pathway plays anti- and pro-tumoral roles in the vast majority of cancers, and long noncoding RNAs have been reported to play key roles in the highly contextual response process. However, the roles of long noncoding RNAs (lncRNAs) in TGF-? signaling in esophageal squamous cell carcinoma (ESCC) remain unknown. In this study, we performed RNA-seq to compare lncRNAs expression levels between TGF-?1-treated and untreated ESCC cells and observed that NF-kappaB-interacting lncRNA (NKILA) was remarkably upregulated by the classical TGF-? signaling pathway. RNA profiling of 39 pairs ESCC tumor and adjacent nontumor samples using RT-qPCR demonstrated that NKILA is significantly downregulated in ESCC tumor tissues, and NKILA expression levels were significantly decreased in advanced tumor tissues (III and IV) compared to early stages (I and II) (p?0.01). Gain- and loss-of-function assays showed that NKILA inhibited ESCC cell metastasis in vitro and in vivo, and mechanism studies showed that NKILA repressed MMP14 expression by inhibiting I?B? phosphorylation and NF-?B activation. Collectively, these findings suggest that the TGF-?-induced lncRNA NKILA has potential as an antimetastasis therapy. Key messages: Long noncoding RNA NKILA could be remarkably upregulated by classical TGF-? signal pathway in ESCC.NKILA was significantly downregulated in esophageal squamous cell carcinoma and negatively correlated with TNM stage.NKILA inhibits ESCC cell metastasis via repressing MMP14 expression by suppressing the phosphorylation of I?B? and NF-?B activation. Electronic supplementary material: The online version of this article (10.1007/s00109-018-1621-1) contains supplementary material, which is available to authorized users.