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敲低通过下调介导的作用抑制急性髓系白血病中的恶性进展。

knockdown inhibits the malignancy progression through downregulating mediated and in acute myeloid leukemia.

作者信息

Ke Shandong, Zhou Xiaofen

机构信息

Department of Hematology, Huangshi Central Hospital, Huangshi 435000, China.

Department of Hematology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang 441021, China.

出版信息

Transl Cancer Res. 2019 Nov;8(7):2526-2534. doi: 10.21037/tcr.2019.10.12.

Abstract

BACKGROUND

This study aimed to investigate the regulatory role of () in the progression of acute myeloid leukemia (AML) and the underlying mechanism.

METHODS

expression was detected in AML cell lines AML-193, KG-1, HL-60, OCI-AML2 and primary normal bone marrow mononuclear cells (BMMC). The effect of knockdown on cell proliferation, apoptosis and expression were detected by transfection of shRNA and control shRNA into KG-1 cells. And the effect of knockdown on , cell proliferation, cell apoptosis as well as potential target genes [ () and ()] in knockdown treated KG-1 cells was assessed by transfection of shRNA and shRNA & shRNA into KG-1 cells.

RESULTS

expression was elevated in AML-193, KG-1, OCI-AML2 cell lines, but similar in HL-60 cell line compared with primary normal BMMC. knockdown inhibited cell proliferation but promoted cell apoptosis in KG-1 cells, meanwhile expression was increased by knockdown in KG-1 cells. And in rescue experiments, knockdown had no effect on expression of , while it increased the expressions of and , promoted cell proliferation, inhibited cell apoptosis in knockdown treated KG-1 cells.

CONCLUSIONS

knockdown inhibits cell proliferation but promotes cell apoptosis via regulating mediated and in AML.

摘要

背景

本研究旨在探讨()在急性髓系白血病(AML)进展中的调节作用及其潜在机制。

方法

检测AML细胞系AML - 193、KG - 1、HL - 60、OCI - AML2及原代正常骨髓单个核细胞(BMMC)中()的表达。通过将()shRNA和对照shRNA转染至KG - 1细胞,检测()敲低对细胞增殖、凋亡及()表达的影响。通过将()shRNA以及()shRNA和()shRNA转染至KG - 1细胞,评估()敲低对()敲低处理的KG - 1细胞中()、细胞增殖、细胞凋亡以及潜在()靶基因[()和()]的影响。

结果

AML - 193、KG - 1、OCI - AML2细胞系中()表达升高,但与原代正常BMMC相比,HL - 60细胞系中()表达相似。()敲低抑制KG - 1细胞增殖但促进细胞凋亡,同时()敲低使KG - 1细胞中()表达增加。在挽救实验中,()敲低对()表达无影响,但增加了()和()的表达,促进了()敲低处理的KG - 1细胞的增殖,抑制了细胞凋亡。

结论

在AML中,()敲低通过调节()介导的()和()抑制细胞增殖但促进细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d971/8799070/16849efbd260/tcr-08-07-2526-f1.jpg

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