MiR-1290 promotes proliferation, migration, and invasion of glioma cells by targeting LHX6

被引:49
|
作者
Yan, Lei [1 ]
Cai, Kerui [1 ]
Sun, Kai [2 ]
Gui, Jinqiu [3 ]
Liang, Jun [1 ]
机构
[1] Mudanjiang Med Univ, Dept Histol & Embryol, 3 Tongxiang Rd, Mudanjiang 157011, Heilongjiang, Peoples R China
[2] Mudanjiang Med Univ, Dept Biol, Mudanjiang, Peoples R China
[3] Mudanjiang Med Univ, Dept Pathogen Microbiol, Mudanjiang, Peoples R China
关键词
glioma; invasion; LHX6; migration; miR-1290; proliferation; LUNG ADENOCARCINOMA; MALIGNANT GLIOMAS; BREAST-CANCER; MICRORNA-1290; GLIOBLASTOMA; EXPRESSION; TISSUES; TUMORS;
D O I
10.1002/jcp.26381
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
To investigate the interaction of miR-1290 and LHX6 in gliomas, and their influence on the propagation and metastasis of glioma cells. The differential expression of miR-1290 in glioma cells was identified by chip screening. The expression level of miR-1290 and LHX6 were determined by qRT-PCR and Western blot. The influence of miR-1290 on propagation of glioma cells were analyzed by MTT assay, EdU incorporation, and colony formation, while the impact of miR-1290 on metastasis was assessed by transwell assay. The relationship between LHX6 and miR-1290 was testified by luciferase reporter assay. The gliomas orthotopic implantation model of nude mice was established to investigate the influence of miR-1290 and LHX6 on tumor growth. Tumor volumes were evaluated by photon density, and the expression of Ki67 protein was analyzed by immunohistochemistry. MiR-1290 presented a higher expression in glioma cells and tissues. MiR-1290 overexpression significantly promoted propagation and metastasis of glioma cells, while miR-1290 knockdown inhibited glioma development. MiR-1290 suppressed LHX6 expression, facilitating development of glioma cells. The orthotopic implantation model showed that miR-1290 overexpression promoted tumor growth while LHX6 overexpression inhibited it. MiR-1290 could promote glioma cell propagation and metastasis by inhibiting LHX6.
引用
收藏
页码:6621 / 6629
页数:9
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