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角蛋白 23 的过表达通过上皮-间充质转化促进卵巢癌细胞的迁移。

The Overexpression of Keratin 23 Promotes Migration of Ovarian Cancer via Epithelial-Mesenchymal Transition.

机构信息

Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100026, China.

出版信息

Biomed Res Int. 2020 Nov 1;2020:8218735. doi: 10.1155/2020/8218735. eCollection 2020.

DOI:10.1155/2020/8218735
PMID:33204716
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7652601/
Abstract

BACKGROUND

Keratin 23 (KRT23) is a new member of the KRT gene family and known to be involved in the development and migration of various types of tumors. However, the role of KRT23 in ovarian cancer (OC) remains unclear. This study is aimed at investigating the function of KRT23 in OC.

METHODS

The expression of KRT23 in normal ovarian and OC tissues was determined using the Oncomine database and immunohistochemical staining. Reverse transcription quantitative polymerase chain reaction assay was used to analyze the expression of KRT23 in normal ovarian epithelial cell lines and OC cell lines. Small interfering RNA (siRNA), wound healing assay, and transwell assay were conducted to detect the effects of KRT23 on OC cell migration and invasion. Further mechanistic studies were verified by the Gene Expression Profiling Interactive Analysis platform, Western blotting, and immunofluorescence staining.

RESULTS

KRT23 was highly expressed in OC tissues and cell lines. High KRT23 expression could regulate OC cell migration and invasion, and the reduction of KRT23 by siRNA inhibited the migration and invasion of OC cells . Furthermore, KRT23 mediated epithelial-mesenchymal transition (EMT) by regulating p-Smad2/3 levels in the TGF-/Smad signaling pathway.

CONCLUSIONS

These results demonstrate that KRT23 plays an important role in OC migration via EMT by regulating the TGF-/Smad signaling pathway.

摘要

背景

角蛋白 23（KRT23）是角蛋白基因家族的新成员，已知其参与多种类型肿瘤的发生和迁移。然而，KRT23 在卵巢癌（OC）中的作用尚不清楚。本研究旨在研究 KRT23 在 OC 中的功能。

方法

使用 Oncomine 数据库和免疫组织化学染色检测正常卵巢组织和 OC 组织中 KRT23 的表达。逆转录定量聚合酶链反应（qRT-PCR）检测正常卵巢上皮细胞系和 OC 细胞系中 KRT23 的表达。通过小干扰 RNA（siRNA）、划痕愈合实验和 Transwell 实验检测 KRT23 对 OC 细胞迁移和侵袭的影响。进一步的机制研究通过基因表达谱交互分析平台、Western blot 和免疫荧光染色进行验证。

结果

KRT23 在 OC 组织和细胞系中高表达。高表达的 KRT23 可调节 OC 细胞的迁移和侵袭，siRNA 降低 KRT23 的表达可抑制 OC 细胞的迁移和侵袭。此外，KRT23 通过调节 TGF-/Smad 信号通路中的 p-Smad2/3 水平介导上皮间质转化（EMT）。

结论

这些结果表明，KRT23 通过调节 TGF-/Smad 信号通路，在 EMT 中通过调节 TGF-/Smad 信号通路在 OC 迁移中发挥重要作用。

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