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Published on: August 28, 2018
EMSY promoted the growth and migration of ovarian cancer cells
Xiaohong Zhao1, Yan Zhou, Mingchao Nie
1Maternal and Child Health Hospital of Hainan Province, 15th South of Longkun Rd, Haikou, 570206, Hainan Province, China.
Abstract:
Epithelial ovarian cancer is one of the most common and aggressive diseases among the female reproductive organ malignancies, and the molecular mechanism underlying this disease remains largely unknown. EMSY, a binding partner of BRCA2, has been reported to be amplified in ovarian cancer. However, the expression pattern and biological functions of EMSY in the progression of ovarian cancer are not fully understood. In this study, it was found that the expression of EMSY was significantly elevated in ovarian cancer samples compared to their adjacent normal tissues. Moreover, overexpression of EMSY promoted the growth and migration of ovarian cancer cells, while knocking down the expression of EMSY inhibited the growth, migration, and tumorigenesis of ovarian cancer cells in vitro and in vivo. Mechanistically, EMSY was found to interact with beta-catenin and activate beta-catenin/TCF signaling. Our study demonstrated that EMSY played an oncogenic role in the progression of ovarian cancer cells and EMSY might be a promising target for the treatment.
Insights
The study found that elevated EMSY expression drives ovarian cancer growth and migration by activating beta-catenin signaling. This suggests EMSY is an oncogene and a potential therapeutic target for epithelial ovarian cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Epithelial ovarian cancer is aggressive with unknown molecular drivers.
- EMSY, a BRCA2 partner, is amplified in ovarian cancer, but its role is unclear.
Purpose of the Study:
- To investigate the expression, function, and mechanism of EMSY in epithelial ovarian cancer progression.
Main Methods:
- Analyzed EMSY expression in ovarian cancer tissues.
- Studied the effects of EMSY overexpression and knockdown on cancer cell growth and migration in vitro and in vivo.
- Investigated EMSY's interaction with beta-catenin and its downstream signaling pathways.
Main Results:
- EMSY expression is significantly higher in ovarian cancer tissues.
- EMSY overexpression promotes ovarian cancer cell growth and migration.
- EMSY knockdown inhibits tumor growth, migration, and tumorigenesis.
- EMSY interacts with beta-catenin, activating the beta-catenin/TCF pathway.
Conclusions:
- EMSY acts as an oncogene in epithelial ovarian cancer progression.
- EMSY signaling is a potential therapeutic target for ovarian cancer treatment.
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