4.2 Article

lncRNA DARS-AS1 Promoted Osteosarcoma Progression through Regulating miR-532-3p/CCR7

期刊

DISEASE MARKERS
卷 2022, 期 -, 页码 -

出版社

HINDAWI LTD
DOI: 10.1155/2022/4660217

关键词

-

向作者/读者索取更多资源

This study firstly suggests that DARS-AS1 acts as an oncogene in osteosarcoma by regulating the miR-532-3p/CCR7 pathway.
Background. lncRNAs have been indicated to involve in cell invasion, proliferation, and metastasis. However, function of DARS-AS1 in osteosarcoma remains poorly explored. Methods. DARS-AS1 and miR-532-3p level were measured using qRT-PCR. CCK-8 assay and cell invasion assay were done to study cell functions. Luciferase reporter assay was performed to study the mechanism about DARS-AS1 and miR-532-3p. Results. We firstly showed that DARS-AS1 expression is upregulated in 73.5% (25/34) of cases with osteosarcoma. Moreover, DARS-AS1 expression is overexpressed in osteosarcoma specimens than in nontumor samples. The DARS-AS1 is overexpressed in the osteosarcoma cell lines (Saos-2, SOSP-9607, U2OS, and MG-63) compared to hFOB. Overexpression of DARS-AS1 promotes cell growth and invasion in MG-63 osteosarcoma cell. DARS-AS1 plays as one sponge for miR-532-3p in osteosarcoma cell, and miR-532-3p overexpression inhibits luciferase activity of DARS-AS1-WT, not DARS-AS1-MUT in MG-63 cell. Ectopic expression of DARS-AS1 inhibits miR-532-3p expression in MG-63 cell. Furthermore, miR-532-3p expression is downregulated in osteosarcoma specimens compared to in paired nontumor samples. MiR-532-3p expression is downregulated in osteosarcoma cell lines compared to hFOB. MiR-532-3p expression is negatively associated with DARS-AS1 expression in osteosarcoma specimens. miR-532-3p directly regulates CCR7 expression in osteosarcoma cell. Elevated DARS-AS1 expression enhances cell growth and invasion via regulating CCR7. Conclusions. These data firstly suggested that DARS-AS1 exerted as one oncogene in osteosarcoma partly via regulating miR-532-3p/CCR7.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.2
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据