Effect arylamine N-acetyltransferase 1 on morphology, adhesion, migration, and invasion of MDA-MB-231 cells: role of matrix metalloproteinases and integrin αV.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2020-12-01 DOI:10.1080/19336918.2019.1710015
Pengcheng Li, Neville J Butcher, Rodney F Minchin
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引用次数: 8

Abstract

Reducted arylamine N-acetyltransferase (NAT1) in breast cancers is associated with poor patient survival. NAT1 has also been associated with changes in cancer cell survival and invasion both invitro and invivo. Here, we report the effects of NAT1 in cancer cell invasion by addressing its role in adherence, migration, and invasion in vitro. The NAT1 gene was deleted in MDA-MB-231, HT-29 and HeLa cells using CRISPR/Cas9 gene editing. Loss of NAT1 increased adherence to collagen in all three cell-lines but migration was unaffected. NAT1 deletion decreased invasion and induced changes to cell morphology. These effects were independent of matrix metalloproteinases but were related to integrin ITGαV expression. The data suggest NAT1 is important in adhesion and invasion through integrin expression.

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芳胺n -乙酰转移酶1对MDA-MB-231细胞形态、粘附、迁移和侵袭的影响:基质金属蛋白酶和整合素αV的作用
乳腺癌中芳胺n -乙酰转移酶(NAT1)的降低与患者生存率低有关。在体外和体内,NAT1也与癌细胞存活和侵袭的变化有关。在这里,我们报告了NAT1在癌细胞侵袭中的作用,通过解决其在体外粘附、迁移和侵袭中的作用。利用CRISPR/Cas9基因编辑技术在MDA-MB-231、HT-29和HeLa细胞中删除NAT1基因。在所有三种细胞系中,NAT1的缺失增加了对胶原蛋白的粘附,但迁移不受影响。NAT1的缺失减少了入侵并诱导了细胞形态的改变。这些作用与基质金属蛋白酶无关,但与整合素itg - α v的表达有关。数据提示NAT1通过整合素的表达在粘附和侵袭中起重要作用。
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CiteScore
7.20
自引率
4.30%
发文量
567
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