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抑癌基因Hes1影响急性髓系白血病细胞增殖和凋亡的机制研究
OBJECTIVE: To elucidate the impact of Hes1 on the proliferation and apoptosis of acute myeloid leukemia (AML) cells. METHODS: The expression levels of Hes1 and p21 in AML patient samples and myeloid leukemia cell lines were analyzed by real-time PCR. Hes1 was up-regulated by retrovirus transfection...
Formato: | Online Artículo Texto |
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Lenguaje: | English |
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Editorial office of Chinese Journal of Hematology
2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343078/ https://www.ncbi.nlm.nih.gov/pubmed/26134013 http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2015.06.008 |
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collection | PubMed |
description | OBJECTIVE: To elucidate the impact of Hes1 on the proliferation and apoptosis of acute myeloid leukemia (AML) cells. METHODS: The expression levels of Hes1 and p21 in AML patient samples and myeloid leukemia cell lines were analyzed by real-time PCR. Hes1 was up-regulated by retrovirus transfection in AML cell lines and the proliferation capacity were assayed by MTT, cell cycle by Hoechst/PY, apoptosis by AnnexinV. RESULTS: The expression of Hes1 in primary AML cells and HL-60、U937、KG1a cell lines were 0.67±0.24, 0.59±0.43, 0.42±0.03, and 0.32±0.26, respectively, and p21 were 0.54±0.01, 0.44±0.12, 0.36±0.12, and 0.59±0.43, respectively. Hes1 expression levels after transduction in HL-60、U937、KG1a were 4.9±0.2, 5.2±0.4, 5.8±0.5, respectively. Induced activation of Hes1 led to AML cells growth arrest and apoptosis, which was associated with an enhanced p21 expression. Besides, activated Hes1 led to AML cells growth inhibition in vivo. CONCLUSION: Hes1 could mediate growth arrest and apoptosis in AML cells, which may be a novel target for AML. |
format | Online Article Text |
id | pubmed-7343078 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Editorial office of Chinese Journal of Hematology |
record_format | MEDLINE/PubMed |
spelling | pubmed-73430782020-07-16 抑癌基因Hes1影响急性髓系白血病细胞增殖和凋亡的机制研究 Zhonghua Xue Ye Xue Za Zhi 论著 OBJECTIVE: To elucidate the impact of Hes1 on the proliferation and apoptosis of acute myeloid leukemia (AML) cells. METHODS: The expression levels of Hes1 and p21 in AML patient samples and myeloid leukemia cell lines were analyzed by real-time PCR. Hes1 was up-regulated by retrovirus transfection in AML cell lines and the proliferation capacity were assayed by MTT, cell cycle by Hoechst/PY, apoptosis by AnnexinV. RESULTS: The expression of Hes1 in primary AML cells and HL-60、U937、KG1a cell lines were 0.67±0.24, 0.59±0.43, 0.42±0.03, and 0.32±0.26, respectively, and p21 were 0.54±0.01, 0.44±0.12, 0.36±0.12, and 0.59±0.43, respectively. Hes1 expression levels after transduction in HL-60、U937、KG1a were 4.9±0.2, 5.2±0.4, 5.8±0.5, respectively. Induced activation of Hes1 led to AML cells growth arrest and apoptosis, which was associated with an enhanced p21 expression. Besides, activated Hes1 led to AML cells growth inhibition in vivo. CONCLUSION: Hes1 could mediate growth arrest and apoptosis in AML cells, which may be a novel target for AML. Editorial office of Chinese Journal of Hematology 2015-06 /pmc/articles/PMC7343078/ /pubmed/26134013 http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2015.06.008 Text en 2015年版权归中华医学会所有 http://creativecommons.org/licenses/by-nc-sa/3.0/ This work is licensed under a Creative Commons Attribution 3.0 License (CC-BY-NC). The Copyright own by Publisher. Without authorization, shall not reprint, except this publication article, shall not use this publication format design. Unless otherwise stated, all articles published in this journal do not represent the views of the Chinese Medical Association or the editorial board of this journal. |
spellingShingle | 论著 抑癌基因Hes1影响急性髓系白血病细胞增殖和凋亡的机制研究 |
title | 抑癌基因Hes1影响急性髓系白血病细胞增殖和凋亡的机制研究 |
title_full | 抑癌基因Hes1影响急性髓系白血病细胞增殖和凋亡的机制研究 |
title_fullStr | 抑癌基因Hes1影响急性髓系白血病细胞增殖和凋亡的机制研究 |
title_full_unstemmed | 抑癌基因Hes1影响急性髓系白血病细胞增殖和凋亡的机制研究 |
title_short | 抑癌基因Hes1影响急性髓系白血病细胞增殖和凋亡的机制研究 |
title_sort | 抑癌基因hes1影响急性髓系白血病细胞增殖和凋亡的机制研究 |
topic | 论著 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343078/ https://www.ncbi.nlm.nih.gov/pubmed/26134013 http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2015.06.008 |
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