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 in vitro. Furthermore, KRT23 mediated epithelial-mesenchymal transition (EMT) by regulating p-Smad2/3 levels in the TGF-β/Smad signaling pathway. Conclusions These results demonstrate that KRT23 plays an important role in OC migration via EMT by regulating the TGF-β/Smad signaling pathway.
Highlights
Ovarian cancer (OC) is one of the most common malignant diseases that threaten the health of women worldwide [1]
The expression of Keratin 23 (KRT23) protein was tested in ten ovarian cancer (OC) tissues and corresponding normal ovarian tissues by immunohistochemistry, and results showed that 70% (10/7) of OC tissues revealed significantly higher staining intensity of KRT23 than normal tissues (Figure 1(b))
The expression of KRT23 was tested in four human OC cell lines (HEY, SKOV3, OVCAR3, and Caov3) by Reverse Transcription Quantitative PCR (RT-qPCR)
Summary
Ovarian cancer (OC) is one of the most common malignant diseases that threaten the health of women worldwide [1]. Previous studies have shown that keratin plays an important role in cell mechanical integrity and barrier function [4]. Several recent studies have reported that abnormal expression of epithelial keratin is associated with the invasion and migration of cancer cells [6,7,8]. 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. The expression of KRT23 in normal ovarian and OC tissues was determined using the Oncomine database and immunohistochemical staining. KRT23 mediated epithelial-mesenchymal transition (EMT) by regulating p-Smad2/3 levels in the TGF-β/Smad signaling pathway. These results demonstrate that KRT23 plays an important role in OC migration via EMT by regulating the TGF-β/Smad signaling pathway
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