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NANOG regulates epithelial-mesenchymal transition and chemoresistance in ovarian cancer
Shan Qin1, Yanfang Li1, Xuexia Cao1
1Department of Obstetrics and Gynecology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Abstract:
A key transcription factor associated with poor prognosis and resistance to chemotherapy in ovarian cancer is NANOG. However, the mechanism by which NANOG functions remains undefined. It has been suggested that epithelial-to-mesenchymal transition (EMT) also contributes to development of drug resistance in different cancers. We thus determined whether NANOG expression was associated with EMT and chemoresistance in epithelial ovarian cancer cells. NANOG expression was increased in epithelial ovarian cancer cell lines compared with its expression in normal epithelial ovarian cell lines. NANOG expression in SKOV-3 or OV2008 cells directly correlated with high expression of mesenchymal cell markers and inversely with low expression of epithelial cell marker. RNAi-mediated silencing of NANOG in SKOV-3 reversed the expression of mesenchymal cell markers and restored expression of E-cadherin. Reversibly, stable overexpression of NANOG in Moody cells increased expression of N-cadherin whereas down-regulating expression of E-cadherin, cumulatively indicating that NANOG plays an important role in maintaining the mesenchymal cell markers. Modulating NANOG expression did not have any effect on proliferation or colony formation. Susceptibility to cisplatin increased in SKOV-3 cells on down-regulating NANOG and reversible results were obtained in Moody cells post-overexpression of NANOG. NANOG silencing in SKOV-3 and OV2008 robustly attenuated in vitro migration and invasion. NANOG expression exhibited a biphasic pattern in patients with ovarian cancer and expression was directly correlated to chemoresistance retrospectively. Cumulatively, our data demonstrate that NANOG expression modulates chemosensitivity and EMT resistance in ovarian cancer.
Insights
NANOG, a key factor in ovarian cancer, drives chemoresistance and epithelial-to-mesenchymal transition (EMT). Silencing NANOG in ovarian cancer cells increased cisplatin sensitivity and reduced migration, highlighting its role in drug resistance.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- NANOG is a transcription factor linked to poor prognosis and chemotherapy resistance in ovarian cancer.
- The precise mechanism of NANOG's function in ovarian cancer, particularly its relationship with epithelial-to-mesenchymal transition (EMT), is not well understood.
- EMT is implicated in the development of drug resistance across various cancer types.
Purpose of the Study:
- To investigate the association between NANOG expression and EMT in epithelial ovarian cancer cells.
- To determine if NANOG influences chemoresistance in ovarian cancer.
- To elucidate the role of NANOG in regulating cellular migration and invasion.
Main Methods:
- Comparison of NANOG expression in ovarian cancer cell lines versus normal epithelial ovarian cell lines.
- Correlation analysis of NANOG expression with epithelial and mesenchymal markers (E-cadherin, N-cadherin) in ovarian cancer cells.
- RNA interference (RNAi)-mediated silencing and stable overexpression of NANOG to assess its functional impact.
- Assessment of cisplatin susceptibility, proliferation, colony formation, migration, and invasion assays.
- Retrospective analysis of NANOG expression in patient samples.
Main Results:
- NANOG expression was elevated in ovarian cancer cell lines compared to normal cells.
- NANOG expression positively correlated with mesenchymal markers and inversely with epithelial markers, indicating a role in EMT.
- NANOG silencing reversed EMT markers and increased cisplatin sensitivity, while overexpression had the opposite effect.
- NANOG modulation did not affect proliferation or colony formation but significantly impacted in vitro migration and invasion.
- Patient data showed a biphasic NANOG expression pattern correlated with chemoresistance.
Conclusions:
- NANOG plays a significant role in maintaining mesenchymal characteristics and promoting EMT in ovarian cancer.
- NANOG expression is a key modulator of chemosensitivity and EMT-driven resistance in ovarian cancer.
- Targeting NANOG may represent a therapeutic strategy to overcome chemoresistance in ovarian cancer.
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