Oncotarget

Research Papers:

Association of the long non-coding RNA MALAT1 with the polycomb repressive complex pathway in T and NK cell lymphoma

Soo Hee Kim, Se Hoon Kim, Woo Ick Yang, Soo Jeong Kim and Sun Och Yoon _

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Oncotarget. 2017; 8:31305-31317. https://doi.org/10.18632/oncotarget.15453

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Abstract

Soo Hee Kim1,2, Se Hoon Kim1, Woo Ick Yang1, Soo Jeong Kim3 and Sun Och Yoon1

1Department of Pathology, Yonsei University College of Medicine, Seoul, Korea

2Anatomic Pathology Reference Lab, Seegene Medical Foundation, Seoul, Korea

3Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea

Correspondence to:

Sun Och Yoon, email: [email protected], [email protected]

Keywords: T and NK cell lymphomas, long non-coding RNA, MALAT1, polycomb repressive complex

Received: June 13, 2016    Accepted: January 31, 2017    Published: February 17, 2017

ABSTRACT

Recently, various long non-coding RNAs (lncRNAs) have been reported to have significant therapeutic or prognostic value. However, the expression of lncRNAs has not been investigated in T and NK cell lymphoma. Thus, we evaluated the biological and prognostic role of lncRNAs related to the polycomb repressive complex (PRC) and PRC markers in tissue samples and cell lines of T and NK cell lymphoma. Among the tested lncRNAs, MALAT1 was most highly expressed in clinical samples and cell lines. High expression of MALAT1 as well as BMI1 was related to poor prognosis in patients with mature T cell lymphoma. In the tissue samples, BMI1 expression showed a positive correlation with EZH2, SUZ12, H3K27me3, and MALAT1. Multiple linear regression analysis showed that BMI1 expression was independently associated with H3K27me3. Direct binding of MALAT1 to the PRC2 components (EZH2 and SUZ12) was observed in a T cell lymphoma cell line; however, no direct binding of MALAT1 with H3K27me3 and BMI1 (a PRC1 component) was observed.

In T and NK cell lymphomas, MALAT1 was related to poor prognosis. MALAT1 directly binds to EZH2 and SUZ12, and BMI1 activation may be induced possibly through H3K27me3.


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