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Published on: January 12, 2020
RPL35A drives ovarian cancer progression by promoting the binding of YY1 to CTCF promoter
Huijuan Wu1, Liangbin Xia2, Lu Sun1
1Department of Gynecological Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China.
Abstract:
Ovarian cancer is one of the most common gynaecological malignancies with poor prognosis and lack of effective treatment. The improvement of the situation of ovarian cancer urgently requires the exploration of its molecular mechanism to develop more effective molecular targeted drugs. In this study, the role of human ribosomal protein l35a (RPL35A) in ovarian cancer was explored in vitro and in vivo. Our data identified that RPL35A expression was abnormally elevated in ovarian cancer. Clinically, high expression of RPL35A predicted short survival and poor TNM staging in patients with ovarian cancer. Functionally, RPL35A knock down inhibited ovarian cancer cell proliferation and migration, enhanced apoptosis, while overexpression had the opposite effect. Mechanically, RPL35A promoted the direct binding of transcription factor YY1 to CTCF in ovarian cancer cells. Consistently, RPL35A regulated ovarian cancer progression depending on CTCF in vitro and in vivo. Furthermore, RPL35A affected the proliferation and apoptosis of ovarian cancer cells through PPAR signalling pathway. In conclusion, RPL35A drove ovarian cancer progression by promoting the binding of YY1 and CTCF promoter, and inhibiting this process may be an effective strategy for targeted therapy of this disease.
Insights
Human ribosomal protein l35a (RPL35A) drives ovarian cancer progression by promoting YY1 and CTCF binding. Inhibiting RPL35A may offer a novel targeted therapy strategy for ovarian cancer patients.
Area of Science:
- Oncology
- Molecular Biology
- Gynaecological Oncology
Background:
- Ovarian cancer is a leading gynaecological malignancy with poor outcomes.
- Effective molecular targeted therapies are needed due to limited treatment options.
- Understanding the molecular mechanisms driving ovarian cancer is crucial.
Purpose of the Study:
- To investigate the role of human ribosomal protein l35a (RPL35A) in ovarian cancer.
- To explore the molecular mechanisms underlying RPL35A's function in ovarian cancer.
- To assess RPL35A as a potential therapeutic target.
Main Methods:
- In vitro and in vivo experiments were conducted.
- RPL35A expression levels were analyzed in ovarian cancer tissues.
- Functional assays included knockdown and overexpression of RPL35A.
- Molecular mechanisms involving transcription factors YY1 and CTCF, and the PPAR signaling pathway were investigated.
Main Results:
- RPL35A expression was significantly elevated in ovarian cancer.
- High RPL35A expression correlated with poor patient survival and advanced TNM staging.
- RPL35A knockdown inhibited cell proliferation and migration, and enhanced apoptosis.
- RPL35A overexpression showed opposite effects.
- RPL35A was found to promote YY1 binding to the CTCF promoter.
- RPL35A regulates ovarian cancer progression via CTCF and the PPAR signaling pathway.
Conclusions:
- RPL35A is a key driver of ovarian cancer progression.
- RPL35A promotes ovarian cancer by facilitating YY1-CTCF binding and influencing the PPAR pathway.
- Targeting RPL35A presents a promising therapeutic strategy for ovarian cancer.
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