Xiao Luo1, Hui Wang2. 1. Department of Breast Surgery, China-Japan Union Hospital of Jilin University, Changchun, 130033, Jilin, China. 2. Department of Ultrasound, China-Japan Union Hospital of Jilin University, Changchun, 130033, Jilin, China. whui66@jlu.edu.cn.
Abstract
BACKGROUND: Long noncoding RNAs (lncRNAs) have recently identified as essential gene modulators in numerous cancers. Previous studies have confirmed the oncogenic role of long intergenic nonprotein-coding RNA 00514 (LINC00514) in some cancers. Nevertheless, its biological function and mechanism remain unclear in triple-negative breast cancer (TNBC). METHODS: Herein, we detected LINC00514 expression level in TNBC tissues and cells using RT-qPCR. The function of LINC00514 in TNBC cellular activities was assessed by colony formation, EdU, wound healing, transwell assays and flow cytometry analysis. RESULTS: The binding between miR-6504-5p/miR-3139 and LINC00514/CCDC71L was validated by luciferase reporter assay. The results indicated that LINC00514 expression was upregulated in TNBC tissues and cells. Furthermore, it was manifested that silenced LINC00514 restrained cell proliferative, migratory and invasive abilities and promoted cell apoptosis. In mechanism, LINC00514 was revealed to sequester miR-6504-5p and miR-3139 in TNBC cells. Furthermore, the low level of miR-6504-5p and miR-3139 was identified in TNBC tissues and cells. Overexpression of miR-6504-5p or miR-3139 inhibited cell growth and migration in TNBC. CCDC71L was recognized as a common downstream gene of miR-6504-5p and miR-3139. Rescue assay verified that overexpressed CCDC71L countervailed the anti-tumor influence of LINC00514 knockdown on TNBC cell proliferation, migration, invasion and apoptosis. CONCLUSIONS: LINC00514 promote cell proliferation, migration and invasion in triple-negative breast cancer by targeting the miR-6504-5p/miR-3139/CCDC71L axis in TNBC.
BACKGROUND: Long noncoding RNAs (lncRNAs) have recently identified as essential gene modulators in numerous cancers. Previous studies have confirmed the oncogenic role of long intergenic nonprotein-coding RNA 00514 (LINC00514) in some cancers. Nevertheless, its biological function and mechanism remain unclear in triple-negative breast cancer (TNBC). METHODS: Herein, we detected LINC00514 expression level in TNBC tissues and cells using RT-qPCR. The function of LINC00514 in TNBC cellular activities was assessed by colony formation, EdU, wound healing, transwell assays and flow cytometry analysis. RESULTS: The binding between miR-6504-5p/miR-3139 and LINC00514/CCDC71L was validated by luciferase reporter assay. The results indicated that LINC00514 expression was upregulated in TNBC tissues and cells. Furthermore, it was manifested that silenced LINC00514 restrained cell proliferative, migratory and invasive abilities and promoted cell apoptosis. In mechanism, LINC00514 was revealed to sequester miR-6504-5p and miR-3139 in TNBC cells. Furthermore, the low level of miR-6504-5p and miR-3139 was identified in TNBC tissues and cells. Overexpression of miR-6504-5p or miR-3139 inhibited cell growth and migration in TNBC. CCDC71L was recognized as a common downstream gene of miR-6504-5p and miR-3139. Rescue assay verified that overexpressed CCDC71L countervailed the anti-tumor influence of LINC00514 knockdown on TNBC cell proliferation, migration, invasion and apoptosis. CONCLUSIONS:LINC00514 promote cell proliferation, migration and invasion in triple-negative breast cancer by targeting the miR-6504-5p/miR-3139/CCDC71L axis in TNBC.