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过表达对胃癌细胞上皮-间充质转化的影响。

Effect of overexpression on epithelial-mesenchymal transition of gastric cancer cells.

机构信息

Department of Surgery, the Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.

Department of Surgery, Xingtai People's Hospital, Hebei Medical University, Xingtai, Hebei, China.

出版信息

J Int Med Res. 2021 Nov;49(11):3000605211051581. doi: 10.1177/03000605211051581.

DOI:10.1177/03000605211051581
PMID:34738482
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8573523/
Abstract

OBJECTIVE

To investigate Krüppel-like factor 17 () expression in normal and gastric cancer tissues and cell lines.

METHODS

Levels of KLF17 mRNA and protein in GES-1 normal gastric mucosal cells, and NCI-N87, SGC-7901, BGC-823 and HGC-27 gastric cancer cells were analysed by quantitative polymerase chain reaction (qPCR) and western blot. Differences in expression between gastric cancer and adjacent tissues were analysed by qPCR and immunohistochemistry. Invasion/migration effects of overexpression in BGC-823 and HGC-27 cells were analysed by wound-healing and Transwell chamber assays. Changes in expression of and epithelial-mesenchymal transition (EMT)-related genes (matrix metalloproteinase [MMP]-9, vimentin and E-cadherin) were analysed in BGC-823 and HGC-27 cells before and after transfection using qPCR and western blot. Transforming growth factor (TGF)-β1, Smad family member (Smad)2/3 and phosphorylated-Smad2/3 levels in BGC-823 and HGC-27 cells were assessed by qPCR and western blot.

RESULTS

expression was lower in gastric cancer versus adjacent tissues, and in gastric cancer cell lines versus GES-1 normal gastric mucosal cells, and was positively correlated with degree of cancer-cell differentiation. Wound-healing and Transwell assays showed decreased migration and invasion ability of BGC-823 and HGC-27 cells transfected to overexpress . overexpression was associated with decreased MMP-9 and vimentin in BGC-823 and HGC-27 cancer cells, and increased KLF17 and E-cadherin. overexpression also resulted in decreased levels of TGF-β1 and p-Smad2/3 in BGC-823 and HGC-27 cancer cells.

CONCLUSION

is poorly expressed in gastric cancer tissues and cell lines. overexpression might inhibit EMT via the TGF-β/Smad pathway, thereby reducing gastric cancer cell invasion and migration. Therefore, KLF17 may become a novel target for treating gastric cancer.

摘要

目的

研究 Krüppel 样因子 17（）在正常胃组织和胃癌组织及细胞系中的表达。

方法

采用实时定量聚合酶链反应（qPCR）和蛋白质印迹法检测 GES-1 正常胃黏膜细胞和 NCI-N87、SGC-7901、BGC-823 和 HGC-27 胃癌细胞中 KLF17 mRNA 和蛋白的水平。qPCR 和免疫组织化学分析胃癌与癌旁组织中表达的差异。划痕愈合和 Transwell 小室实验分析 BGC-823 和 HGC-27 细胞中过表达对侵袭/迁移的影响。qPCR 和蛋白质印迹法分析 BGC-823 和 HGC-27 细胞转染前后 KLF17 和上皮-间充质转化（EMT）相关基因（基质金属蛋白酶[MMP]-9、波形蛋白和 E-钙黏蛋白）的表达变化。qPCR 和蛋白质印迹法评估 BGC-823 和 HGC-27 细胞中转化生长因子（TGF）-β1、Smad 家族成员（Smad）2/3 和磷酸化-Smad2/3 的水平。

结果

与癌旁组织相比，胃癌组织中表达降低，与 GES-1 正常胃黏膜细胞相比，胃癌细胞系中表达降低，且与癌细胞分化程度呈正相关。划痕愈合和 Transwell 实验显示，过表达的 BGC-823 和 HGC-27 细胞迁移和侵袭能力降低。BGC-823 和 HGC-27 癌细胞中过表达与 MMP-9 和波形蛋白降低，KLF17 和 E-钙黏蛋白增加有关。BGC-823 和 HGC-27 癌细胞中 TGF-β1 和 p-Smad2/3 水平降低与过表达有关。

结论

在胃癌组织和细胞系中表达水平较低。过表达可能通过 TGF-β/Smad 通路抑制 EMT，从而降低胃癌细胞的侵袭和迁移。因此，KLF17 可能成为治疗胃癌的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/2dc07fd3e978/10.1177_03000605211051581-fig13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/7409ba4d6ba0/10.1177_03000605211051581-fig1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/095c305a6547/10.1177_03000605211051581-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/cb02cc8f9999/10.1177_03000605211051581-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/418a95e7638e/10.1177_03000605211051581-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/5690269bc66d/10.1177_03000605211051581-fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/72c114f8269c/10.1177_03000605211051581-fig11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/a6c1047fa97f/10.1177_03000605211051581-fig12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/2dc07fd3e978/10.1177_03000605211051581-fig13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/7409ba4d6ba0/10.1177_03000605211051581-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/c0bb6040ae31/10.1177_03000605211051581-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/783cc0473892/10.1177_03000605211051581-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/c1828c803e99/10.1177_03000605211051581-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/a8ead6557ed0/10.1177_03000605211051581-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/27b222d30447/10.1177_03000605211051581-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/095c305a6547/10.1177_03000605211051581-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/cb02cc8f9999/10.1177_03000605211051581-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/418a95e7638e/10.1177_03000605211051581-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/5690269bc66d/10.1177_03000605211051581-fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/72c114f8269c/10.1177_03000605211051581-fig11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/a6c1047fa97f/10.1177_03000605211051581-fig12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09ff/8573523/2dc07fd3e978/10.1177_03000605211051581-fig13.jpg

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