The long non-coding RNA LINC01013 enhances invasion of human anaplastic large-cell lymphoma.
The long non-coding RNA LINC01013 enhances invasion of human anaplastic large-cell lymphoma.
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DOI：
10.1038/s41598-017-00382-7
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发表时间：
2017-03-22
影响因子：
4.6
通讯作者：
Lin KH
中科院分区：
文献类型：
--
作者：
Chung IH;Lu PH;Lin YH;Tsai MM;Lin YW;Yeh CT;Lin KH
间变性大细胞淋巴瘤（ALCL）是一种罕见的高度恶性非霍奇金淋巴瘤。目前，只有关于嵌合癌基因NPM-ALK的研究报道了与ALCL进展的联系。然而，ALCL侵袭的具体分子机制尚不清楚。在这里，我们试图研究ALCL中差异表达的长链非编码rna （lncRNAs）及其潜在的生物学功能。我们的微阵列分析显示，一种新的非编码RNA基因LINC01013在ALCL临床标本中高表达，并在侵袭性ALCL细胞系中显著上调。敲低LINC01013抑制肿瘤细胞侵袭；相反，它的过表达增强了肿瘤细胞的侵袭。linc01013诱导的侵袭是通过激活上皮-间质转化（EMT）相关蛋白、蜗牛蛋白和纤维连接蛋白介导的。具体而言，LINC01013诱导蜗牛，导致纤维连接蛋白激活，增强ALCL细胞侵袭。总之，这些发现支持LINC01013通过蜗牛-纤维连接蛋白激活级联在癌细胞侵袭中的潜在作用，并表明LINC01013可能被用作ALCL的转移标志物。
Anaplastic large-cell lymphoma (ALCL) is a rare type of highly malignant, non-Hodgkin lymphoma (NHL). Currently, only studies on the chimeric oncogene NPM-ALK have reported a link to ALCL progression. However, the specific molecular mechanisms underlying the invasion of ALCL are still unclear. Here, we sought to investigate differentially expressed, long non-coding RNAs (lncRNAs) in ALCL and their potential biological function. Our microarray analyses revealed that LINC01013, a novel non-coding RNA gene, was highly expressed in clinical specimens of ALCL and was significantly upregulated in invasive ALCL cell lines. Knockdown of LINC01013 suppressed tumor cell invasion; conversely, its overexpression enhanced tumor cell invasion. LINC01013-induced invasion was mediated by activation of the epithelial-to-mesenchymal transition (EMT)-associated proteins, snail and fibronectin. Specifically, LINC01013 induced snail, resulting in activation of fibronectin and enhanced ALCL cell invasion. Collectively, these findings support a potential role for LINC01013 in cancer cell invasion through the snail-fibronectin activation cascade and suggest that LINC01013 could potentially be utilized as a metastasis marker in ALCL.