The long non-coding RNA LINC01013 enhances invasion of human anaplastic large-cell lymphoma

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,...

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Vydáno v:Scientific reports Ročník 7; číslo 1; s. 295 - 10
Hlavní autoři: Chung, I-Hsiao, Lu, Pei-Hsuan, Lin, Yang-Hsiang, Tsai, Ming-Ming, Lin, Yun-Wen, Yeh, Chau-Ting, Lin, Kwang-Huei
Médium: Journal Article
Jazyk:angličtina
Vydáno: London Nature Publishing Group UK 22.03.2017
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ISSN:2045-2322, 2045-2322
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Shrnutí: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.
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ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-017-00382-7