LncRNAITGB2-AS1 Could Promote the Migration and Invasion of Breast Cancer Cells through Up-Regulating ITGB2

被引:58
|
作者
Liu, Mengyao [1 ]
Gou, Liyao [1 ]
Xia, Jing [1 ]
Wan, Qun [1 ]
Jiang, Yayun [1 ]
Sun, Shilei [1 ]
Tang, Min [1 ]
He, Tongchuan [2 ]
Zhang, Yan [1 ]
机构
[1] Chongqing Med Univ, Chinese Minist Educ, Key Lab Diagnost Med, Chongqing 400000, Peoples R China
[2] Univ Chicago, Med Ctr, Dept Surg, Mol Oncol Lab, Chicago, IL 60637 USA
关键词
lncRNA; ITGB2-AS1; ITGB2; breast cancer; migration; invasion; OPEN PLATFORM; METASTASIS; LANDSCAPE; LNCRNAS; GROWTH;
D O I
10.3390/ijms19071866
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In the previous study, we screened a novel lncRNA-ITGB2-AS1, which was down-regulated by bone morphogenetic protein 9 (BMP9) in breast cancer cell. Studying ITGB2-AS1 will lay the foundation for the exploring mechanism of the BMP9 inhibitory effect on breast cancer. The expression analysis related to ITGB2-AS1 in clinical samples was conducted on online websites. The overexpression plasmid or siRNA fragment was transfected into breast cancer cells to alter its gene expression. The MTT assay and flow cytometry were used to measure cell viability and cell cycle. Additionally, cell migration and invasion were detected by wound healing and transwell assay. The results of biological function experiments showed that ITGB2-AS1 could promote the migration and invasion of breast cancer. Furthermore, ITGB2-AS1 increased the mRNA and protein expression of ITGB2. Consistent with ITGB2-AS1, ITGB2 exerted the promotion effect on the migration and invasion of breast cancer and activated integrin-related FAK signaling. The OL plasmid expressing the truncation of ITGB2-AS1, which was complementary to ITGB2, was essential for activation of FAK signaling. In conclusion, LncRNA ITGB2-AS1 could promote the migration and invasion of breast cancer cells by up-regulating ITGB2.
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页数:13
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