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Overexpression of the long non-coding RNA PVT1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia

BACKGROUND: Acute promyelocytic leukemia (APL) is associated with chromosomal translocation t(15;17), which results in the proliferation of morphologically abnormal promyelocytes. Gain of supernumerary copies of the 8q24 chromosomal region, which harbors MYC and PVT1, has been shown to be the most c...

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Autores principales: Zeng, Chengwu, Yu, Xibao, Lai, Jing, Yang, Lijiang, Chen, Shaohua, Li, Yangqiu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4636781/
https://www.ncbi.nlm.nih.gov/pubmed/26545364
http://dx.doi.org/10.1186/s13045-015-0223-4
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author Zeng, Chengwu
Yu, Xibao
Lai, Jing
Yang, Lijiang
Chen, Shaohua
Li, Yangqiu
author_facet Zeng, Chengwu
Yu, Xibao
Lai, Jing
Yang, Lijiang
Chen, Shaohua
Li, Yangqiu
author_sort Zeng, Chengwu
collection PubMed
description BACKGROUND: Acute promyelocytic leukemia (APL) is associated with chromosomal translocation t(15;17), which results in the proliferation of morphologically abnormal promyelocytes. Gain of supernumerary copies of the 8q24 chromosomal region, which harbors MYC and PVT1, has been shown to be the most common secondary alteration in human APL. Increased MYC can accelerate the development of myeloid leukemia in APL. However, the role that the expression of the long non-coding RNA (lncRNA) PVT1 plays in the pathogenesis of APL remains largely unknown. FINDINGS: In this study, we first analyzed the lncRNA PVT1 expression level in peripheral blood cells from 28 patients with de novo APL, and significantly upregulated PVT1 was found in APL patients compared with healthy donors. We then observed significantly lower MYC and PVT1 expression during all-trans retinoic acid (ATRA)-induced differentiation and cell cycle arrest in the APL cell line. MYC knockdown in NB4 cells led to PVT1 downregulation. Moreover, PVT1 knockdown by RNA interference led to suppression of the MYC protein level, and cell proliferation was inhibited. CONCLUSION: Our findings reveal that the lncRNA PVT1 may play an important role in the proliferation of APL cells and may be useful for future therapeutic management. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13045-015-0223-4) contains supplementary material, which is available to authorized users.
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spelling pubmed-46367812015-11-08 Overexpression of the long non-coding RNA PVT1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia Zeng, Chengwu Yu, Xibao Lai, Jing Yang, Lijiang Chen, Shaohua Li, Yangqiu J Hematol Oncol Rapid Communication BACKGROUND: Acute promyelocytic leukemia (APL) is associated with chromosomal translocation t(15;17), which results in the proliferation of morphologically abnormal promyelocytes. Gain of supernumerary copies of the 8q24 chromosomal region, which harbors MYC and PVT1, has been shown to be the most common secondary alteration in human APL. Increased MYC can accelerate the development of myeloid leukemia in APL. However, the role that the expression of the long non-coding RNA (lncRNA) PVT1 plays in the pathogenesis of APL remains largely unknown. FINDINGS: In this study, we first analyzed the lncRNA PVT1 expression level in peripheral blood cells from 28 patients with de novo APL, and significantly upregulated PVT1 was found in APL patients compared with healthy donors. We then observed significantly lower MYC and PVT1 expression during all-trans retinoic acid (ATRA)-induced differentiation and cell cycle arrest in the APL cell line. MYC knockdown in NB4 cells led to PVT1 downregulation. Moreover, PVT1 knockdown by RNA interference led to suppression of the MYC protein level, and cell proliferation was inhibited. CONCLUSION: Our findings reveal that the lncRNA PVT1 may play an important role in the proliferation of APL cells and may be useful for future therapeutic management. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13045-015-0223-4) contains supplementary material, which is available to authorized users. BioMed Central 2015-11-06 /pmc/articles/PMC4636781/ /pubmed/26545364 http://dx.doi.org/10.1186/s13045-015-0223-4 Text en © Zeng et al. 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Rapid Communication
Zeng, Chengwu
Yu, Xibao
Lai, Jing
Yang, Lijiang
Chen, Shaohua
Li, Yangqiu
Overexpression of the long non-coding RNA PVT1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia
title Overexpression of the long non-coding RNA PVT1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia
title_full Overexpression of the long non-coding RNA PVT1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia
title_fullStr Overexpression of the long non-coding RNA PVT1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia
title_full_unstemmed Overexpression of the long non-coding RNA PVT1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia
title_short Overexpression of the long non-coding RNA PVT1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia
title_sort overexpression of the long non-coding rna pvt1 is correlated with leukemic cell proliferation in acute promyelocytic leukemia
topic Rapid Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4636781/
https://www.ncbi.nlm.nih.gov/pubmed/26545364
http://dx.doi.org/10.1186/s13045-015-0223-4
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