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Cancer Biol Ther. 2017 Jun 3;18(6):414-424. doi: 10.1080/15384047.2017.1323585. Epub 2017 Jun 14.

Elevation of MiR-9-3p suppresses the epithelial-mesenchymal transition of nasopharyngeal carcinoma cells via down-regulating FN1, ITGB1 and ITGAV.

Author information

1
a Department of Reproductive Medicine , The Affiliated Hospital of Qingdao University , Qingdao , Shandong , China.
2
b Department of Radiology , Yuhuangding Hospital of Yantai , Yantai , Shandong , China.
3
c Department of Laboratory Medicine , Central Hospital of Qingdao , Qingdao , Shandong , China.
4
d Department of Radiology , People's Hospital of Zhangqiu , Zhangqiu , Jinan , China.
5
e Department of Oncology , Jining No.1 People's Hospital , Jining , Shandong , China.

Abstract

MicroRNAs had been proved to be pivotal regulators in nasopharyngeal carcinoma (NPC) by regulating a large amount of genes' expression. In our research, we aim to explore the functions of miR-9-3p on the metastases of NPC and figure out the potential mechanisms. First, we revealed downregulation of miR-9-3p and upregulation of fibronectin 1 (FN1), β1 integrin (ITGB1) and α5 integrin (ITGAV) expression in NPC tissues and cells compared with the normal using RNA-seq analysis, RT-qPCR, western blot and immunohistochemistry. By transfection of miR-9-3p mimics in CNE-1, CNE-2 and HONE-1 cells, we confirmed tumor-suppressing roles of miR-9-3p via suppressing EMT process by MTT, wound scratch, transwell assay and western blot. After constructing luciferase reporting plasmids and transient transfection in HEK 293T cells, we proved that FN1, ITGB1 and ITGAV were all targets of miR-9-3p. Then we manipulated the expression of miR-9-3p, FN1, ITGB1 and ITGAV in HONE-1 cells, verifying the tumor-promoting effect of FN1, ITGB1 and ITGAV on cell proliferation and metastases via facilitating EMT process of cells. Additionally, these functions of FN1, ITGB1 and ITGAV could be efficiently abrogated by overexpression of miR-9-3p. Taken together, we demonstrated that elevation of miR-9-3p suppresses the proliferation and metastases of NPC via downregulating FN1, ITGB1, ITGAV and inhibiting the EMT process, which provided a series of therapeutic targets for the treatment of NPC.

KEYWORDS:

FN1; ITGAV; ITGB1; miR-9–3p; nasopharyngeal carcinoma

PMID:
28613134
PMCID:
PMC5536934
DOI:
10.1080/15384047.2017.1323585
[Indexed for MEDLINE]
Free PMC Article

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