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Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
GRIM19 is involved in WT1 expression and epithelial-to-mesenchymal transition in adenomyotic lesions
Chen Geng1, Hao-Ran Liu1, Yue Zhao1
1Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Abstract:
The epithelial-to-mesenchymal transition may play a role in adenomyosis. GRIM19 expression is downregulated in adenomyotic lesions, and the effects of this downregulation in adenomyosis remain relatively unclear. In this study, we aimed to explore whether aberrant GRIM19 expression is associated with the epithelial-to-mesenchymal transition in adenomyosis and found that the expression of both GRIM19 and WT1 was low, and epithelial-to-mesenchymal transition, which included significant changes in CDH1, CDH2 and KRT8 expression, occurred in adenomyotic lesions, as confirmed by Western blotting and quantitative real-time PCR. We provided novel insights into WT1 expression in adenomyosis, revealing that WT1 expression was increased in the endometrial glands of adenomyotic lesions by immunohistochemistry. In vitro, knockdown of GRIM19 expression by small interfering RNA (siRNA) promoted the proliferation, migration and invasion of Ishikawa cells, as measured by Cell Counting Kit-8, wound healing assay and Transwell assays. Western blotting and quantitative real-time PCR confirmed that WT1 expression increased and epithelial-to-mesenchymal transition was induced, including the upregulation of CDH2 and downregulation of CDH1 and KRT8after transfecting the GRIM19 siRNA to Ishikawa cells. Furthermore, WT1 expression was upregulated and epithelial-to-mesenchymal transition was observed, including downregulation of CDH1 and KRT8in GRIM19 gene-knockdown mice. Upregulation of Wt1 expression in the endometrial glands of Grim19 knockdown mice was also verified by immunohistochemistry. Taken together, these results reveal that low expression of GRIM19 in adenomyosis may upregulate WT1 expression and induce epithelial-to-mesenchymal transition in the endometria, providing new insights into the pathogenesis of adenomyosis.
Insights
Low GRIM19 expression in adenomyosis may trigger WT1 upregulation, promoting epithelial-to-mesenchymal transition (EMT). This finding offers new insights into adenomyosis pathogenesis and potential therapeutic targets for this condition.
Area of Science:
- Gynecologic pathology
- Cellular biology
- Molecular mechanisms of disease
Background:
- Adenomyosis is a gynecologic disorder where the endometrium implants within the uterine myometrium.
- Epithelial-to-mesenchymal transition (EMT) is implicated in adenomyosis pathogenesis.
- GRIM19 (Gene Regulation: Interferon-induced 19) expression is reduced in adenomyosis, but its role is unclear.
Purpose of the Study:
- To investigate the association between GRIM19 downregulation and EMT in adenomyosis.
- To explore the role of WT1 (Wilms Tumor 1) in this process.
Main Methods:
- Western blotting and quantitative real-time PCR to assess gene and protein expression (GRIM19, WT1, CDH1, CDH2, KRT8).
- Immunohistochemistry to localize WT1 expression in human and mouse tissues.
- In vitro studies using Ishikawa cells with GRIM19 knockdown via siRNA.
- In vivo studies using GRIM19 gene-knockdown mice.
Main Results:
- Adenomyotic lesions showed decreased GRIM19 and increased WT1 expression.
- EMT markers (CDH1, CDH2, KRT8) were altered, indicating EMT occurrence in adenomyosis.
- GRIM19 knockdown in vitro and in vivo promoted cell proliferation, migration, and invasion.
- GRIM19 knockdown led to increased WT1 expression and induced EMT in Ishikawa cells and mouse models.
Conclusions:
- Downregulation of GRIM19 in adenomyosis may upregulate WT1 expression.
- This upregulation of WT1 appears to induce EMT in endometrial cells.
- These findings provide novel insights into adenomyosis pathogenesis and suggest GRIM19/WT1 pathways as potential therapeutic targets.
