MicroRNA-128 promotes apoptosis in lung cancer by directly targeting NIMA-related kinase 2.

Abstract:

BACKGROUND:MicroRNA-128 (miR-128) serves as a regulator by inducing cancer cell apoptosis, differentiation, the epithelial-to-mesenchymal transition process, and tumor growth by mediating different targets. NIMA-related kinase 2 (NEK2) is aberrantly expressed in lung cancer. The miR-128/NEK2 pathway has been reported to predict prognosis in colorectal cancer; however, the determination of a relationship between miR-128 and NEK2 in lung cancer has remained elusive. We explored the association between miR-128 and NEK2 in lung cancer. METHODS:MiR-128 and NEK2 expression were examined in 15 lung cancer tissues by real time-PCR. Lung cancer SK-MES-1 cells were transfected with miR-128 mimic, an inhibitor or a negative control. MiR-128 and NEK2 expression levels were detected using quantitative real time-PCR and Western blot. SK-MES-1 cell apoptosis was performed by flow cytometry. RESULTS:Compared to adjacent non-tumor tissues, miR-128 was downregulated and NEK2 was upregulated in 15 lung cancer tissues. Lung cancer SK-MES-1 cells transfected with miR-128 mimic induced a higher apoptotic rate than those transfected with the negative control. Dual luciferase assay further confirmed that NEK2 was a direct target of miR-128 in lung cancer, and transfection with miR-128 mimic could decrease the NEK2 protein level while the miR-128 inhibitor increased NEK2 expression. Finally, the apoptotic effect of lung cancer cells induced by miR-128 mimic could be reversed by NEK2 overexpression. CONCLUSIONS:NEK2 was regulated by miR-128 in lung cancer and miR-128 induced lung cancer cell apoptosis by mediating NEK2 expression.

journal_name

Thorac Cancer

journal_title

Thoracic cancer

authors

Zhao D,Han W,Liu X,Cui D,Chen Y

doi

10.1111/1759-7714.12442

subject

Has Abstract

pub_date

2017-07-01 00:00:00

pages

304-311

issue

4

eissn

1759-7706

issn

1759-7714

journal_volume

8

pub_type

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