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MiR-99a-5p regulates proliferation, migration and invasion abilities of human oral carcinoma cells by targeting NOX4

In: NEOPLASMA, vol. 64, no. 5
Y. Shi - Z. Bo - G. Pang - X. Qu - W. Bao - L. Yang - Y. Ma
Detaily:
Rok, strany: 2017, 666 - 673
O článku:
Previous research has showed that miR-99a-5p was a tumor suppressor. The aim of our study was to explore the effect of miR-99a-5p on the vitality and proliferation, migration together with the invasion of oral tumor cells via inhibiting the expression of NOX4. QRT-PCR and Western blot were applied to examine the expression level of miR-99a-5p and NOX4 in human oral tumorous and adjacent tissues. Dual luciferase reporter gene assay was applied to confirm that miR-99a-5p negatively regulated directly on NOX4 in TSCC1 cells. Cell transfection and lentiviral vectors were used to up-regulate expression of miR-99a-5p and NOX4, respectively. Cell proliferation, cell cycle, apoptosis and invasion along with the migration in different groups were assessed using MTT assay, colony formation assay, the flow cytometry, transwell assay and the wound healing assay, respectively. MiR-99a-5p was under-expressed in human oral tumor, while NOX4 was over-expressed. There was a negative relationship between miR-99a-5p and NOX4. Up-regulating miR-99a-5p or down-regulating NOX4 suppressed the vitality, proliferation, migration together with invasion of TSCC1 cells. MiR-99a-5p affected the vitality and proliferation, migration together with the invasion of oral tumor cells through targeting NOX4. Keywords: oral carcinoma, miR-99a-5p, NOX4
Ako citovať:
ISO 690:
Shi, Y., Bo, Z., Pang, G., Qu, X., Bao, W., Yang, L., Ma, Y. 2017. MiR-99a-5p regulates proliferation, migration and invasion abilities of human oral carcinoma cells by targeting NOX4. In NEOPLASMA, vol. 64, no.5, pp. 666-673. 0028-2685.

APA:
Shi, Y., Bo, Z., Pang, G., Qu, X., Bao, W., Yang, L., Ma, Y. (2017). MiR-99a-5p regulates proliferation, migration and invasion abilities of human oral carcinoma cells by targeting NOX4. NEOPLASMA, 64(5), 666-673. 0028-2685.