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Original Research Article | OPEN ACCESS

Effect of miR-200c on nasopharyngeal carcinoma and the probable molecular regulatory mechanism involved

Sheng Xu1, Wenxia He2

11Department of Otorhinolaryngology, Maternal and Child Health Hospital of Hubei Province, Wuhan 430070; 2Department of Otorhinolaryngology, The People's Hospital of China Three Gorges University & The First People’s Hospital of Yichang, Yichang 443000, PR China.

For correspondence:-  Wenxia He   Email: ugyt0p@163.com

Accepted: 28 December 2020        Published: 31 January 2021

Citation: Xu S, He W. Effect of miR-200c on nasopharyngeal carcinoma and the probable molecular regulatory mechanism involved. Trop J Pharm Res 2021; 20(1):41-46 doi: 10.4314/tjpr.v20i1.7

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To determine the effect of micro-ribonucleic acid-200c (miR-200c) on biological function of nasopharyngeal carcinoma, and the likely molecular regulatory mechanism involved.
Methods: Thirty (30) nasopharyngeal carcinoma tissues and para-cancerous normal tissues were taken from patients undergoing surgery in Maternal and Child Health Hospital of Hubei Province, Wuhan from September 2018 to January 2020. The expression levels of miR-200c in the two types of tissues were determined. Cells of human nasopharyngeal carcinoma cell line HNE1 were cultured to about 70 % growth prior to transfection with blank plasmid, PINI and miR-200c analogs. After 48 h of culture, control group, PINI group, and miR-200c over-expression + PINI group were obtained. The expression levels of PINI and changes in centrosomes in each group were measured, and changes in cell migration in each group were determined using Transwell migration assay.
Results: Compared with para-cancerous normal tissues, the expression level of miR-200c in nasopharyngeal carcinoma was significantly increased (p < 0.01). Compared with the control group, the PINI expression level and cell migration ability in miR-200c overexpression tissue were markedly decreased, while the percentage of extra centrosomes was markedly increased. Compared to miR-200c over-expression tissue, the PINI expression level and cell migration ability in the miR-200c over-expression + PINI group were markedly raised, while the percentage of extra-central somatic cells was significantly decreased (p < 0.05).
Conclusion: MiR-200c may inhibit the migration of nasopharyngeal carcinoma cells by inhibiting the expression of PINI and inhibiting abnormal expansion of centrosomes.

Keywords: MiR-200c, Nasopharyngeal carcinoma, Biological function, Molecular regulatory mechanism

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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