LncRNA SNHG11 aggravates cell proliferation and migration in triple-negative breast cancer via sponging miR-2355-5p and targeting CBX5

LncRNA SNHG11 通过海绵 miR-2355-5p 和靶向 CBX5 加剧三阴性乳腺癌细胞增殖和迁移

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作者:Lei Yu, Wei Zhang, Peng Wang, Qi Zhang, Aihua Cong, Xiuyuan Yang, Kai Sang

Abstract

Triple-negative breast cancer (TNBC) is one of the most common malignances worldwide. Concurrently, the incidence of TNBC has continued to rise in recent years. It is reported that long non-coding RNAs (lncRNAs) are involved in biological processes in numerous cancers including TNBC. Small nucleolar RNA host gene 11 (SNHG11) has already been studied and reported in some cancers. However, the role of SNHG11 in TNBC remains unknown. RT-qPCR was used to measure gene expression in the current study. CCK-8, colony formation, flow cytometry, Transwell and western blotting experiments were also performed to determine the biological function of SNHG11 in TNBC cells. Luciferase reporter and RIP assays were performed to measure relationship between genes. In the present study, the results indicated SNHG11 was highly expressed in TNBC tissues and cell lines. Moreover, SNHG11 aggravated cell proliferation and migration, and whereas it attenuated cell apoptosis in TNBC. Furthermore, SNHG11 sponged microRNA 2355-5p (miR-2355-5p) in TNBC. Silencing SNHG11 increased miR-2355-5p expression. In addition, chromobox 5 (CBX5) was identified to be targeted by miR-2355-5p in TNBC. It was also suggested that CBX5 silencing suppressed cell proliferation and migration. Furthermore, overexpressed CBX5 recovered the inhibitive influence of SNHG11 silencing on proliferative and migrative abilities of TNBC cells. Overall, SNHG11 acted as a tumor promoter in TNBC and regulated TNBC cell growth by modulating the miR-2355-5p/CBX5 axis, which indicated that it may be used as a biomarker for TNBC treatment.

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