Proliferation mechanism of acute myeloid leukemia cell line GDM-1 with CSF1R-Y571D mutation

Objective To explore the proliferation mechanism of acute myeloid leukemia cell line GDM-1 by the method of protein kinase inhibition. Methods GDM-1 cells were divided into experimental group and control group according to different treatment. Experimental group was treated with 10 different prote...

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Main Author: CAO Qiong, XU Ning-xin, LI Xiao-wen, WU Hao, HAO Jian-qing, QIN Yan-hong, LI Li
Format: Article
Language:zho
Published: Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College. 2021-01-01
Series:Jichu yixue yu linchuang
Subjects:
Online Access:http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/a191312.pdf
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author CAO Qiong, XU Ning-xin, LI Xiao-wen, WU Hao, HAO Jian-qing, QIN Yan-hong, LI Li
author_facet CAO Qiong, XU Ning-xin, LI Xiao-wen, WU Hao, HAO Jian-qing, QIN Yan-hong, LI Li
author_sort CAO Qiong, XU Ning-xin, LI Xiao-wen, WU Hao, HAO Jian-qing, QIN Yan-hong, LI Li
collection DOAJ
description Objective To explore the proliferation mechanism of acute myeloid leukemia cell line GDM-1 by the method of protein kinase inhibition. Methods GDM-1 cells were divided into experimental group and control group according to different treatment. Experimental group was treated with 10 different protein kinase inhibitors, the control group was treated with DMSO, and the inhibition of cell proliferation was detected by CCK8 method. The phosphorylation level of key protein kinases in GDM-1 after treatment with linifanib, bosutinib, sorafenib were detected by Western blot.GDM-1 cells were treated with cytokine M-CSF alone or combined with protein kinase inhibitors, cell proliferation was detected by CCK8 method. Results Protein kinase inhibition analysis showed that dasatinib (IC50=0.01 μmol/L), bosutinib(IC50=0.07 μmol/L), linifanib (IC50=0.13 μmol/L) and sorafenib (IC50= 0.12 μmol/L) significantly inhibited the proliferation of GDM-1 cells. Western blot analysis showed that the phosphorylation level of Src and ERK in GDM-1 was decreased (P<0.01) when treated with linifaninb. The proliferation of GDM-1 was 11.3 times as much as that of control group when stimulated with M-CSF. The proliferation of GDM-1 was dramatically inhibited when incubated with the combination of M-CSF and bosutinib (P<0.001), but it was not significantly inhibited when incubated with M-CSF plus HG6-64-1. Conclusions CSF1R-Y571D mutation of GDM-1 cells increases the activity of CSF1R, and promotes cell proliferation by activating Src and MAPK signaling pathways.
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spelling doaj.art-18a75898448b477babab45259d949d112024-01-05T03:04:13ZzhoInstitute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College.Jichu yixue yu linchuang1001-63252021-01-014114449Proliferation mechanism of acute myeloid leukemia cell line GDM-1 with CSF1R-Y571D mutationCAO Qiong, XU Ning-xin, LI Xiao-wen, WU Hao, HAO Jian-qing, QIN Yan-hong, LI Li01. School of Basic Medicine, Shanxi Medical University, Taiyuan 030001; ;2. Department of Hematology, the Second Hospital of Shanxi Medical University, Taiyuan 030001, ChinaObjective To explore the proliferation mechanism of acute myeloid leukemia cell line GDM-1 by the method of protein kinase inhibition. Methods GDM-1 cells were divided into experimental group and control group according to different treatment. Experimental group was treated with 10 different protein kinase inhibitors, the control group was treated with DMSO, and the inhibition of cell proliferation was detected by CCK8 method. The phosphorylation level of key protein kinases in GDM-1 after treatment with linifanib, bosutinib, sorafenib were detected by Western blot.GDM-1 cells were treated with cytokine M-CSF alone or combined with protein kinase inhibitors, cell proliferation was detected by CCK8 method. Results Protein kinase inhibition analysis showed that dasatinib (IC50=0.01 μmol/L), bosutinib(IC50=0.07 μmol/L), linifanib (IC50=0.13 μmol/L) and sorafenib (IC50= 0.12 μmol/L) significantly inhibited the proliferation of GDM-1 cells. Western blot analysis showed that the phosphorylation level of Src and ERK in GDM-1 was decreased (P<0.01) when treated with linifaninb. The proliferation of GDM-1 was 11.3 times as much as that of control group when stimulated with M-CSF. The proliferation of GDM-1 was dramatically inhibited when incubated with the combination of M-CSF and bosutinib (P<0.001), but it was not significantly inhibited when incubated with M-CSF plus HG6-64-1. Conclusions CSF1R-Y571D mutation of GDM-1 cells increases the activity of CSF1R, and promotes cell proliferation by activating Src and MAPK signaling pathways.http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/a191312.pdfprotein kinase inhibitor|gdm-1|colony stimulating factor-1 receptor|linifanib|bosutinib
spellingShingle CAO Qiong, XU Ning-xin, LI Xiao-wen, WU Hao, HAO Jian-qing, QIN Yan-hong, LI Li
Proliferation mechanism of acute myeloid leukemia cell line GDM-1 with CSF1R-Y571D mutation
Jichu yixue yu linchuang
protein kinase inhibitor|gdm-1|colony stimulating factor-1 receptor|linifanib|bosutinib
title Proliferation mechanism of acute myeloid leukemia cell line GDM-1 with CSF1R-Y571D mutation
title_full Proliferation mechanism of acute myeloid leukemia cell line GDM-1 with CSF1R-Y571D mutation
title_fullStr Proliferation mechanism of acute myeloid leukemia cell line GDM-1 with CSF1R-Y571D mutation
title_full_unstemmed Proliferation mechanism of acute myeloid leukemia cell line GDM-1 with CSF1R-Y571D mutation
title_short Proliferation mechanism of acute myeloid leukemia cell line GDM-1 with CSF1R-Y571D mutation
title_sort proliferation mechanism of acute myeloid leukemia cell line gdm 1 with csf1r y571d mutation
topic protein kinase inhibitor|gdm-1|colony stimulating factor-1 receptor|linifanib|bosutinib
url http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/a191312.pdf
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