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LINC00221 suppresses the malignancy of children acute lymphoblastic leukemia

As the most common malignant disease in childhood, children acute lymphoblastic leukemia (ALL) is a heterogeneous disease caused by the accumulated genetic alterations. Long non-coding RNAs (lncRNAs) are reported as critical regulators in diseases. GEPIA database indicated that long intergenic non-p...

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Autores principales: Huang, Man, Zheng, Jiajia, Ren, Yongya, Zhu, Jingjing, Kou, Linbing, Nie, Jinhong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7199449/
https://www.ncbi.nlm.nih.gov/pubmed/32297639
http://dx.doi.org/10.1042/BSR20194070
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author Huang, Man
Zheng, Jiajia
Ren, Yongya
Zhu, Jingjing
Kou, Linbing
Nie, Jinhong
author_facet Huang, Man
Zheng, Jiajia
Ren, Yongya
Zhu, Jingjing
Kou, Linbing
Nie, Jinhong
author_sort Huang, Man
collection PubMed
description As the most common malignant disease in childhood, children acute lymphoblastic leukemia (ALL) is a heterogeneous disease caused by the accumulated genetic alterations. Long non-coding RNAs (lncRNAs) are reported as critical regulators in diseases. GEPIA database indicated that long intergenic non-protein coding RNA 221 (LINC00221) was conspicuously down-regulated in acute myeloid leukemia. However, its expression pattern in ALL has not been revealed. This work was carried out to study the role of LINC00221 in ALL cells. Quantitative real-time PCR (qRT-PCR) quantified LINC00221 expression in ALL cells. The function of LINC00221 in ALL was determined by ki-67 immunofluorescence staining, EdU, TUNEL, JC-1, and caspase-3/8/9 activity assays. RNA pull down and Ago2-RNA immunoprecipitation (RIP) assays investigated the interaction between miR-152-3p and LINC00221 or ATPase sarcoplasmic/endoplasmic reticulum Ca2(+) transporting 2 (ATP2A2). Our study revealed the low expression of LINC00221 in ALL cells. Subsequently, LINC00221 was verified to bind with miR-152-3p. Moreover, functional assays pointed out that LINC00221 overexpression posed anti-proliferation and pro-apoptosis effects in ALL cells, and these effects could be separately reversed by miR-152-3p up-regulation. Afterward, LINC00221 was revealed to regulate ATP2A2 expression via sponging miR-152-3p. Additionally, ATP2A2 was verified to involve in regulating LINC00221-mediated ALL cell proliferation and apoptosis. In conclusion, LINC00221 suppressed ALL cell proliferation and boosted ALL cell apoptosis via sponging miR-152-3p to up-regulate ATP2A2.
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spelling pubmed-71994492020-05-13 LINC00221 suppresses the malignancy of children acute lymphoblastic leukemia Huang, Man Zheng, Jiajia Ren, Yongya Zhu, Jingjing Kou, Linbing Nie, Jinhong Biosci Rep Cancer As the most common malignant disease in childhood, children acute lymphoblastic leukemia (ALL) is a heterogeneous disease caused by the accumulated genetic alterations. Long non-coding RNAs (lncRNAs) are reported as critical regulators in diseases. GEPIA database indicated that long intergenic non-protein coding RNA 221 (LINC00221) was conspicuously down-regulated in acute myeloid leukemia. However, its expression pattern in ALL has not been revealed. This work was carried out to study the role of LINC00221 in ALL cells. Quantitative real-time PCR (qRT-PCR) quantified LINC00221 expression in ALL cells. The function of LINC00221 in ALL was determined by ki-67 immunofluorescence staining, EdU, TUNEL, JC-1, and caspase-3/8/9 activity assays. RNA pull down and Ago2-RNA immunoprecipitation (RIP) assays investigated the interaction between miR-152-3p and LINC00221 or ATPase sarcoplasmic/endoplasmic reticulum Ca2(+) transporting 2 (ATP2A2). Our study revealed the low expression of LINC00221 in ALL cells. Subsequently, LINC00221 was verified to bind with miR-152-3p. Moreover, functional assays pointed out that LINC00221 overexpression posed anti-proliferation and pro-apoptosis effects in ALL cells, and these effects could be separately reversed by miR-152-3p up-regulation. Afterward, LINC00221 was revealed to regulate ATP2A2 expression via sponging miR-152-3p. Additionally, ATP2A2 was verified to involve in regulating LINC00221-mediated ALL cell proliferation and apoptosis. In conclusion, LINC00221 suppressed ALL cell proliferation and boosted ALL cell apoptosis via sponging miR-152-3p to up-regulate ATP2A2. Portland Press Ltd. 2020-05-04 /pmc/articles/PMC7199449/ /pubmed/32297639 http://dx.doi.org/10.1042/BSR20194070 Text en © 2020 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).
spellingShingle Cancer
Huang, Man
Zheng, Jiajia
Ren, Yongya
Zhu, Jingjing
Kou, Linbing
Nie, Jinhong
LINC00221 suppresses the malignancy of children acute lymphoblastic leukemia
title LINC00221 suppresses the malignancy of children acute lymphoblastic leukemia
title_full LINC00221 suppresses the malignancy of children acute lymphoblastic leukemia
title_fullStr LINC00221 suppresses the malignancy of children acute lymphoblastic leukemia
title_full_unstemmed LINC00221 suppresses the malignancy of children acute lymphoblastic leukemia
title_short LINC00221 suppresses the malignancy of children acute lymphoblastic leukemia
title_sort linc00221 suppresses the malignancy of children acute lymphoblastic leukemia
topic Cancer
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7199449/
https://www.ncbi.nlm.nih.gov/pubmed/32297639
http://dx.doi.org/10.1042/BSR20194070
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