4.6 Article

Apatinib inhibits cell proliferation and migration of osteosarcoma via activating LINC00261/miR-620/PTEN axis

期刊

CELL CYCLE
卷 20, 期 18, 页码 1785-1798

出版社

TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2021.1949132

关键词

Apatinib; LINC00261; miR-620; osteosarcoma; PTEN

向作者/读者索取更多资源

Apatinib inhibits the proliferation and migration of osteosarcoma cells through the LINC00261/miR-620/PTEN axis, indicating its potential therapeutic efficacy.
Apatinib has been recently identified as a potential treatment option for osteosarcoma (OS). Nonetheless, the molecular mechanism of Apatinib in regulating OS progression remains unclear. To explore the downstream molecules that mediated the tumor-suppressive effect of Apatinib on OS. Expression levels of genes were detected by RT-qPCR and western blot assays. Functional assays including Transwell assay were applied to detect the proliferation, apoptosis and migration of OS cells. Molecular interactions were detected by luciferase reporter assay and RIP assay. Apatinib inhibited the proliferation and migration of OS cells. LINC00261 was down-regulated in OS cells but then up-regulated after the treatment by Apatinib. Silencing LINC00261 abrogated the suppressive effect of Apatinib on OS cell proliferation and migration. MicroRNA-620 (miR-620) could be sponged by LINC00261. Besides, miR-620 was up-regulated in OS cells and Apatinib treatment reduced miR-620 expression. Furthermore, LINC00261 acted as a competitive endogenous RNA (ceRNA) by sequestering miR-620 to up-regulate the expression of phosphatase and tensin homolog (PTEN). Moreover, Apatinib hindered in vitro cell proliferation and migration as well as the in vivo tumorigenesis of OS through LINC00261/miR-620/PTEN axis. Apatinib-enhanced LINC00261 restrained OS via miR-620/PTEN axis, indicating LINC00261 might promote the efficacy of Apatinib on OS.

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

4.6
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