In:
Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics, Computers, Materials and Continua (Tech Science Press), Vol. 26, No. 3 ( 2018-04-10), p. 385-400
Abstract:
Many studies have shown that downregulation of miR-138 occurs in a variety of cancers including non-small cell lung cancer (NSCLC). However, the precise mechanisms of miR-138 in NSCLC have not been well clarified. In this study, we investigated the biological functions and molecular
mechanisms of miR-138 in NSCLC cell lines, discussing whether it could turn out to be a therapeutic biomarker of NSCLC in the future. In our study, we found that miR-138 is downregulated in NSCLC tissues and cell lines. Moreover, the low level of miR-138 was associated with increased expression of SOX4 in NSCLC tissues and cell lines. Upregulation of miR-138 significantly inhibited proliferation of NSCLC cells. In addition, invasion and EMT of NSCLC cells were suppressed by overexpression of miR-138. However, downregulation of miR-138 promoted cell growth and metastasis of NSCLC
cells. Bioinformatics analysis predicted that SOX4 was a potential target gene of miR-138. Next, luciferase reporter assay confirmed that miR-138 could directly target SOX4. Consistent with the effect of miR-138, downregulation of SOX4 by siRNA inhibited proliferation, invasion, and EMT of NSCLC cells. Overexpression of SOX4 in NSCLC cells partially reversed the effect of miR-138 mimic. In addition, decreased SOX4 expression could increase the level of miR-138 via upregulation of p53. Introduction of miR-138 dramatically inhibited growth, invasion, and EMT of NSCLC cells through
a SOX4/p53 feedback loop.
Type of Medium:
Online Resource
ISSN:
0965-0407
DOI:
10.3727/096504017X14973124850905
Language:
English
Publisher:
Computers, Materials and Continua (Tech Science Press)
Publication Date:
2018
detail.hit.zdb_id:
1114699-0
detail.hit.zdb_id:
2044620-2
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