Open AccessSilencing of lncRNA CCDC26 Restrains the Growth and Migration of Glioma Cells In Vitro and In Vivo via Targeting miR-203
Author(s) -
Shilei Wang,
Yuzuo Hui,
Xiaoming Li,
Qingbin Jia
Publication year - 2018
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504017x14965095236521
Subject(s) - gene silencing , glioma , transfection , cancer research , cell growth , in vivo , apoptosis , downregulation and upregulation , microrna , cell culture , viability assay , cell , biology , small interfering rna , chemistry , biochemistry , gene , genetics , microbiology and biotechnology
Gliomas are the most common primary brain tumors with high mortality. The treatment for gliomas is largely limited due to its uncomprehending pathological mechanism. Here we aimed to investigate the effect of long noncoding RNA (lncRNA) coiled-coil domain-containing 26 (CCDC26) in glioma progression. In our study, the expression of CCDC26 was found upregulated in glioma tissues and cell lines compared with normal tissues and cell lines. Further exploration detected decreased cell proliferation and increased cell apoptosis in U-251 and M059J cells transfected with CCDC26-siRNA. In addition, the silencing of CCDC26 strongly reduced the wound closing rate and the number of invasive cells compared with the scramble group. Simultaneously, the expression of miR-203 was found suppressed in glioma tissues and cells lines. Suppressed level of miR-203 was then elevated in U-251 and M059J cells transfected with CCDC26-siRNA. The result of the luciferase activity assay also showed that the luciferase activity was strongly strengthened by adding the miR-203 inhibitor into the CCDC26 WT group. Moreover, CDCC26-siRNA counteracted the effect of the miR-203 inhibitor in facilitating cell viability and mobility in U-251 cells. The in vivo experiment also revealed that CCDC26-siRNA inhibited glioma growth and metastasis. Taken together, our research indicated a CCDC26/miR-203 pathway in regulating the growth and metastasis of gliomas, providing new viewpoints and promising targets for glioma therapy.