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NOL6 Promotes Tumor Progression by Facilitating Cancer Cell-Induced Platelet Aggregation and Angiogenesis in Breast
Tingting Zhang1, Cheng Lu2, Mingming Lv2
1Department of General Surgery, Lianyungang Affiliated Hospital of Nanjing University of Traditional Chinese Medicine, 222000 Lianyungang, Jiangsu, China.
Frontiers in Bioscience (Landmark Edition)
|March 28, 2025
Summary
Nucleolar protein 6 (NOL6) promotes breast cancer progression by enhancing platelet aggregation and angiogenesis. Targeting NOL6 may offer new therapeutic strategies for breast cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Breast cancer (BC) is a leading malignancy in women, with platelet aggregation implicated in its progression.
- Identifying novel therapeutic targets for BC is crucial for improving patient outcomes.
- Nucleolar protein 6 (NOL6) is a potential target, located on chromosome 9p13 and linked to tumor development.
Purpose of the Study:
- To investigate NOL6 expression in breast cancer.
- To examine the role of NOL6 in platelet aggregation and angiogenesis.
- To elucidate the molecular mechanisms underlying NOL6's function in BC progression.
Main Methods:
- Bioinformatic analyses, qPCR, and immunoblotting assessed NOL6 expression.
- Cell proliferation assays (CCK-8, EdU) evaluated NOL6's impact on BC cells.
- Immunostaining, ELISA, FCM, and in vivo tumor assays investigated NOL6's role in platelet aggregation, angiogenesis, and tumor growth.
Main Results:
- NOL6 expression is elevated in BC and correlates with prognosis, platelet aggregation, and angiogenesis.
- NOL6 knockdown reduced BC cell proliferation, platelet aggregation, angiogenesis, and migration.
- In vivo studies confirmed NOL6 promotes tumor growth.
Conclusions:
- NOL6 promotes breast cancer progression by enhancing platelet aggregation and angiogenesis.
- The Twist1/galectin-3 axis is a key mechanism through which NOL6 exerts its effects.
- NOL6 represents a potential therapeutic target for breast cancer.
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