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Published on: January 12, 2020
N-myc downstream regulated gene 1 acts as a tumor suppressor in ovarian cancer
Bei Wang1, Jianli Li2, Zhanying Ye2
1Hebei Medical University, Shijiazhuang, Hebei 050017, P.R. China.
Abstract:
Although implicated in a number of tumor types, the role of N-myc downstream regulated gene 1 (NDRG1) in ovarian cancer (OC) is unclear. In the present study, we used short hairpin RNA (shRNA) to silence NDRG1 in the OC cell line OVCAR3 and assessed the effect of its knockdown on cell morphology, proliferation, colony formation, migration and invasion. To complement these knockdown studies, we overexpressed NDRG1 in the same cell line. We found that NDRG1 knockdown significantly enhanced OVCAR3 proliferation, migration and invasion; however, there were no apparent changes in cell morphology. We also examined the effect in vivo and found that NDRG1 depletion promoted OVCAR3 xenograft growth in nude mice. In accordance with these data, we found that NDRG1 overexpression decreased proliferation, adhesion and apoptosis, and induced G0/G1 cell cycle arrest in OVCAR3 cells; expression of p21 and p53 was also increased. In conclusion, we demonstrated that NDRG1 acts as a tumor suppressor in ovarian carcinogenesis and may be a potential therapeutic target in this disease.
Insights
N-myc downstream regulated gene 1 (NDRG1) acts as a tumor suppressor in ovarian cancer. Silencing NDRG1 promoted tumor growth, while its overexpression inhibited it, suggesting NDRG1 as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- The role of N-myc downstream regulated gene 1 (NDRG1) in ovarian cancer (OC) remains unclear despite its implication in various tumor types.
- Understanding NDRG1's function is crucial for developing targeted therapies for ovarian cancer.
Purpose of the Study:
- To investigate the role of NDRG1 in ovarian cancer progression.
- To assess the impact of NDRG1 modulation (silencing and overexpression) on ovarian cancer cell behavior.
- To evaluate NDRG1 as a potential therapeutic target in ovarian carcinogenesis.
Main Methods:
- Utilized short hairpin RNA (shRNA) to silence NDRG1 in the OVCAR3 ovarian cancer cell line.
- Overexpressed NDRG1 in the OVCAR3 cell line to complement knockdown studies.
- Assessed effects on cell morphology, proliferation, colony formation, migration, invasion, adhesion, apoptosis, and cell cycle.
- Evaluated in vivo effects using OVCAR3 xenograft models in nude mice.
Main Results:
- NDRG1 knockdown significantly enhanced OVCAR3 cell proliferation, migration, and invasion.
- NDRG1 depletion promoted OVCAR3 xenograft tumor growth in vivo.
- NDRG1 overexpression decreased proliferation, adhesion, and apoptosis.
- NDRG1 overexpression induced G0/G1 cell cycle arrest and increased p21 and p53 expression.
Conclusions:
- NDRG1 functions as a tumor suppressor in ovarian cancer development.
- Modulating NDRG1 levels impacts ovarian cancer cell behavior and tumor growth.
- NDRG1 represents a potential therapeutic target for ovarian cancer treatment.
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