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Original Articles

Hsa-miR-372-5p regulates the NIMA related kinase 7 and IL-1β release in NK/T-cell lymphoma

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Pages 2648-2656 | Received 13 Nov 2020, Accepted 19 May 2021, Published online: 03 Jun 2021
 

Abstract

Epstein-Barr virus (EBV) infection is prevalent and associated with distinct diseases including infectious mononucleosis (IM), chronic active EBV infection (CAEBV) and NK/T-cell lymphoma (NKTL). However, the specific roles of EBV in these diseases remain unclear. Here, the whole miRNA expression datasets derived from 7 IM, 6 CAEBV, and 3 NKTL biopsies were obtained. Homo sapiens microRNA-372-5p (Hsa-miR-372-5p) was upregulated in both CAEBV and NKTL patients. Overexpression of hsa-miR-372-5p altered the expression of over 100 proteins. In addition, hsa-miR-372-5p may target NIMA related kinase 7 to regulate NLRP3 inflammasome activation in host cell. Taken together, we reported different miRNA expression profiles in distinct EBV associated diseases, which provided novel insights to understand how host miRNAs contribute to the mechanism of EBV associated diseases. Hsa-miR-372-5p, as well as other differential expressed miRNA, might serve as potential targets in the therapy of various EBV associated diseases.

Ethics approval and consent to participate

All EBV patients received general supportive treatments at the Department of Hematology, Peking University Shenzhen Hospital. Informed consent forms were obtained from all patients. All procedures performed in studies involving human participants were approved by the Institutional Review Board of Peking University Shenzhen Hospital and in accordance with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Author contributions

Qi Chen: Investigation, Writing – Original Draft. Shenglin Liu: Data Curation, Validation. Kaoyuan Zhang: Software. Bo Yu: Formal analysis. Wei Zhang: Resources. Hongyu Zhang: Conceptualization, Supervision. Xiaofan Chen: Methodology, Writing – Review and Editing.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by National Natural Science Foundation of China [31601172, 81874249], Guangdong Basic and Applied Basic Research Foundation [2016A030310069, 2020A1515011125, 2021A1515012185, 2021A1515011558], Shenzhen High-level Hospital Construction Fund, Sanming Project of Medicine in Shenzhen [SZSM201612004], Shenzhen Science and Technology Innovation Committee International Cooperative Research Project [GJHZ20180420180752400], Shenzhen Research Grant [JCYJ20170411090739316, JCYJ20170306161807726, JCYJ20180507182657867, JCYJ20180223181224405].

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