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Clinical significance of Wip1 overexpression and its association with the p38MAPK/p53/p16 pathway in NSCLC.
- Source :
-
Molecular medicine reports [Mol Med Rep] 2017 Feb; Vol. 15 (2), pp. 719-723. Date of Electronic Publication: 2016 Dec 13. - Publication Year :
- 2017
-
Abstract
- Wip1 is deregulated in numerous human malignancies. However, its roles in non‑small cell lung cancer (NSCLC) remain unclear. In the current study, the expression of Wip1 was investigated in NSCLC and its clinical significance was detected. Immunohistochemical staining was used to measure the expression of (wild‑type p53 induced phosphatase 1) Wip1, p38 mitogen‑activated protein kinase (MAPK), p53, p16 protein in a group of 60 NSCLC and 20 normal lung tissues. In addition, western blotting was performed to detect the Wip1 protein in fresh tissues. The correlations between clinical characteristics and Wip1 expression were analyzed using SPSS, version 16.0 software. The expression of Wip1 was positive in 63.3% (38/60) of NSCLC tissues, and in none of the normal lung tissues (0/20; P<0.01). In addition, Wip1 overexpression was significantly associated with tumor length and differentiation (P=0.008 and 0.03, respectively). The expression of Wip1 was negatively correlated with that of p38MAPK, p53 and p16 (r=‑0.284, ‑0.352 and ‑0.348, respectively). The results of the current study demonstrated that Wip1 was frequently overexpressed in NSCLC, which may serve an essential role in the p38MAPK/p53/p16 signaling pathway.
- Subjects :
- Adult
Aged
Carcinoma, Non-Small-Cell Lung metabolism
Cell Line, Tumor
Female
Gene Expression
Humans
Immunohistochemistry
Lung Neoplasms metabolism
Male
Middle Aged
Neoplasm Staging
Signal Transduction
Carcinoma, Non-Small-Cell Lung physiopathology
Cyclin-Dependent Kinase Inhibitor p16 metabolism
Lung Neoplasms physiopathology
Protein Phosphatase 2C genetics
Protein Phosphatase 2C metabolism
Tumor Suppressor Protein p53 metabolism
p38 Mitogen-Activated Protein Kinases metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1791-3004
- Volume :
- 15
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Molecular medicine reports
- Publication Type :
- Academic Journal
- Accession number :
- 27959454
- Full Text :
- https://doi.org/10.3892/mmr.2016.6032