Eukaryotic initiation factor 3B downregulation suppresses cell proliferation, migration and invasion while it induces cell apoptosis by blocking the β-catenin pathway in endometrial cancer
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1Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, China.
Abstract:
This study aimed to evaluate the effect of eukaryotic initiation factor 3B (EIF3B) downregulation on cell proliferation, apoptosis, migration, invasion and the β-catenin pathway in endometrial cancer. EIF3B mRNA and protein expressions were determined in human endometrial cancer cell lines (Ishikawa, HEC-1A, RL95-2 and EFE-184) and in the normal human endometrial epithelial cell line (HEEC). EIF3B siRNA and a control siRNA were transfected into HEC-1A cells, then cell proliferation, apoptosis, apoptotic marker (C-caspase 3 and Bcl-2) expressions, cell migration, and invasion were determined. β-catenin and cyclin E1 (CCNE1) expressions were also measured. EIF3B mRNA and protein expressions were increased in the Ishikawa, HEC-1A and RL95-2 cell lines, but they were similar in the EFE-184 cell line compared to the HEEC cell line. In HEC-1A cells, EIF3B siRNA suppressed cell proliferation, but it elevated the cell apoptosis rate compared to the control siRNA, and EIF3B siRNA also enhanced C-caspase 3 expression, but it inhibited Bcl-2 expression. Also, EIF3B siRNA reduced cell migration and cell invasion compared to the control siRNA in HEC-1A cells. More interestingly, EIF3B siRNA reduced β-catenin and CCNE1 mRNA as well as protein expressions compared with the control siRNA in HEC-1A cells. In conclusion, EIF3B downregulation suppresses cell proliferation, migration, and invasion, but it induces cell apoptosis by blocking the β-catenin pathway in endometrial cancer.
Insights
Downregulating eukaryotic initiation factor 3B (EIF3B) in endometrial cancer cells inhibits proliferation, migration, and invasion. This downregulation also induces apoptosis by impacting the beta-catenin pathway.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Endometrial cancer is a significant gynecological malignancy.
- Eukaryotic initiation factor 3B (EIF3B) is implicated in cancer progression.
- The role of EIF3B in endometrial cancer requires further elucidation.
Purpose of the Study:
- To investigate the impact of EIF3B downregulation on endometrial cancer cell behavior.
- To assess the effect of EIF3B on proliferation, apoptosis, migration, and invasion.
- To explore the relationship between EIF3B and the beta-catenin pathway in endometrial cancer.
Main Methods:
- EIF3B expression analysis in endometrial cancer cell lines.
- Transfection of EIF3B siRNA in HEC-1A cells.
- Assessment of cell proliferation, apoptosis, migration, and invasion.
- Measurement of beta-catenin and cyclin E1 (CCNE1) expression levels.
Main Results:
- EIF3B expression was elevated in several endometrial cancer cell lines.
- EIF3B downregulation suppressed proliferation, migration, and invasion in HEC-1A cells.
- EIF3B siRNA treatment increased apoptosis and modulated apoptotic markers (C-caspase 3, Bcl-2).
- EIF3B downregulation reduced beta-catenin and CCNE1 expression.
Conclusions:
- EIF3B plays a crucial role in promoting endometrial cancer cell growth and metastasis.
- EIF3B downregulation presents a potential therapeutic strategy for endometrial cancer.
- Targeting EIF3B may be effective through the modulation of the beta-catenin pathway.
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