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자료유형
학술저널
저자정보
Liqiang Qi (Department of Breast Surgical Oncology Cancer Institute and Cancer Hospital Chinese Academy of Medi) Bo Sun (The 2nd Department of Breast Cancer Tianjin Medical University Cancer Institute and Hospital Tianji) Beibei Yang (The 2nd Department of Breast Cancer Tianjin Medical University Cancer Institute and Hospital Tianji) Su Lu (The 2nd Department of Breast Cancer Tianjin Medical University Cancer Institute and Hospital Tianji)
저널정보
한국유방암학회 Journal of Breast Cancer Journal of Breast Cancer Vol.24 No.5
발행연도
2021.10
수록면
428 - 442 (15page)
DOI
10.4048/jbc.2021.24.e42

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Purpose Triple-negative breast cancer (TNBC) is a subtype of breast cancer. Increasing evidence supports that dysregulation of long noncoding RNAs (lncRNAs) plays a vital role in cancer progression. RNA component of mitochondrial RNA processing endoribonuclease (RMRP), a lncRNA, is characterized as a tumor-propeller in some cancers, but its mechanism in TNBC remains poorly understood. This study aimed to determine whether and how RMRP functions in TNBC. Methods Cell proliferation was determined by cell counting kit-8 (CCK-8) and colony formation assays and cell apoptosis by flow cytometry analysis and terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) assay. Cell migration and invasion were determined by transwell assays. RNA-binding protein immunoprecipitation (RIP), luciferase reporter, and RNA pulldown assays were implemented to assess the interaction of RMRP with other molecules in TNBC cells. Results RMRP expression was elevated in TNBC cells. RMRP knockdown repressed cell proliferation, migration, and invasion, but induced apoptosis in TNBC. In addition, RMRP was found to target microRNA-766-5p (miR-766-5p) in TNBC cells. Silencing miR-766-5p enhanced cell viability and decreased apoptosis, whereas miR-766-5p overexpression had opposite effects. Furthermore, miR-766-5p was found to bind to yes-associated protein 1 (YAP1). Moreover, miR-766-5p inhibition reversed the repressive effect of RMRP knockdown on the malignant progression of TNBC. Conclusion The present study manifested that RMRP promotes the growth, migration, and invasion of TNBC cells via the miR-766-5p/YAP1 axis. These findings provide novel perspectives for TNBC treatment.

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