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miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma

BACKGROUND: miR-101 is reported to be associated with cell proliferation and apoptosis. However, it is unknown whether miR-101 expression affects cell proliferation and apoptosis in diffuse large B cell lymphoma (DLBCL). The aim of the present study was to investigate the expression of miR-101 and i...

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Autores principales: Huang, Yiqun, Zou, Yong, Lin, Luhui, Ma, Xudong, Zheng, Ruiji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6455001/
https://www.ncbi.nlm.nih.gov/pubmed/31040714
http://dx.doi.org/10.2147/CMAR.S197744
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author Huang, Yiqun
Zou, Yong
Lin, Luhui
Ma, Xudong
Zheng, Ruiji
author_facet Huang, Yiqun
Zou, Yong
Lin, Luhui
Ma, Xudong
Zheng, Ruiji
author_sort Huang, Yiqun
collection PubMed
description BACKGROUND: miR-101 is reported to be associated with cell proliferation and apoptosis. However, it is unknown whether miR-101 expression affects cell proliferation and apoptosis in diffuse large B cell lymphoma (DLBCL). The aim of the present study was to investigate the expression of miR-101 and its effect on cell proliferation and apoptosis in DLBCL. METHODS: miR-101 expression was detected in 30 cases of patients with DLBCL and normal lymph node by qRT-PCR. Then, miR-101 expression was up-regulated and down-regulated in Originated Cell Line-Large Lymphoma 8 (OCL-LY8) cell line, respectively. MTT and flow cytometry assay were used to evaluate the effect of miR-101 on cell proliferation and apoptosis, respectively. As KDM1A was confirmed to be as a specific target of miR-101 by TargetScanHuman, the relationship between MiR-101 and KDM1A was further investigated. RESULTS: miR-101 expression in patients with DLBCL was significantly reduced compared those in normal lymph node (P<0.05). miR-101 expression was significantly associated with tumor size, clinical stage and International Prognostic Index (IPI) scores (P<0.05). In OCL-LY8 cell line, miR-101 down-regulation significantly promoted cell proliferation and suppressed cell apoptosis. Meanwhile, miR-101 up-regulation reversed this effect. In addition, miR-101 negatively regulated the expression of KDM1A. KDM1A down-regulation was oberved in normal tissues compared with those in DLBCL tissues, which inhibited cell proliferation and promoted cell apoptosis. CONCLUSION: These data indicate that miR-101 regulates cell proliferation and apoptosis by targeting KDM1A, which provides a potential therapeutic for DLBCL patients.
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spelling pubmed-64550012019-04-30 miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma Huang, Yiqun Zou, Yong Lin, Luhui Ma, Xudong Zheng, Ruiji Cancer Manag Res Original Research BACKGROUND: miR-101 is reported to be associated with cell proliferation and apoptosis. However, it is unknown whether miR-101 expression affects cell proliferation and apoptosis in diffuse large B cell lymphoma (DLBCL). The aim of the present study was to investigate the expression of miR-101 and its effect on cell proliferation and apoptosis in DLBCL. METHODS: miR-101 expression was detected in 30 cases of patients with DLBCL and normal lymph node by qRT-PCR. Then, miR-101 expression was up-regulated and down-regulated in Originated Cell Line-Large Lymphoma 8 (OCL-LY8) cell line, respectively. MTT and flow cytometry assay were used to evaluate the effect of miR-101 on cell proliferation and apoptosis, respectively. As KDM1A was confirmed to be as a specific target of miR-101 by TargetScanHuman, the relationship between MiR-101 and KDM1A was further investigated. RESULTS: miR-101 expression in patients with DLBCL was significantly reduced compared those in normal lymph node (P<0.05). miR-101 expression was significantly associated with tumor size, clinical stage and International Prognostic Index (IPI) scores (P<0.05). In OCL-LY8 cell line, miR-101 down-regulation significantly promoted cell proliferation and suppressed cell apoptosis. Meanwhile, miR-101 up-regulation reversed this effect. In addition, miR-101 negatively regulated the expression of KDM1A. KDM1A down-regulation was oberved in normal tissues compared with those in DLBCL tissues, which inhibited cell proliferation and promoted cell apoptosis. CONCLUSION: These data indicate that miR-101 regulates cell proliferation and apoptosis by targeting KDM1A, which provides a potential therapeutic for DLBCL patients. Dove Medical Press 2019-04-05 /pmc/articles/PMC6455001/ /pubmed/31040714 http://dx.doi.org/10.2147/CMAR.S197744 Text en © 2019 Huang et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Huang, Yiqun
Zou, Yong
Lin, Luhui
Ma, Xudong
Zheng, Ruiji
miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma
title miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma
title_full miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma
title_fullStr miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma
title_full_unstemmed miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma
title_short miR-101 regulates cell proliferation and apoptosis by targeting KDM1A in diffuse large B cell lymphoma
title_sort mir-101 regulates cell proliferation and apoptosis by targeting kdm1a in diffuse large b cell lymphoma
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6455001/
https://www.ncbi.nlm.nih.gov/pubmed/31040714
http://dx.doi.org/10.2147/CMAR.S197744
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