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High expression of monocarboxylate transporter 4 predicts poor prognosis in patients with lung adenocarcinoma.

Authors :
YUSHU RUAN
FANJUN ZENG
ZHIQIANG CHENG
XIANDA ZHAO
PIN FU
HONGLEI CHEN
Source :
Oncology Letters. Nov2017, Vol. 14 Issue 5, p5727-5734. 8p.
Publication Year :
2017

Abstract

Monocarboxylate transporter 4 (MCT-4) serves a key function in transporting lactate across the plasma membrane in various types of human cancer. Evidence indicates that MCT-4 expression is associated with non-small cell lung cancer; however, the distribution and clinical significance of MCT-4 in the lung adenocarcinoma (AC) subtype remain unknown. Thus, the aim of the present study was to explore the clinicopathological significance and prognostic values of MCT-4 expression in lung AC. Quantum dots-based immunofluorescence histochemistry was performed to observe the expression of MCT-4 in 146 specimens of lung AC and corresponding normal lung tissues. MCT-4 protein and mRNA were detected by western blotting and reverse transcription- quantitative polymerase chain reaction from 30 fresh samples of lung AC and corresponding normal lung tissues. Of the 146 samples, 25 (17.1%) exhibited high and 121 (82.9%) exhibited low MCT-4 expression. MCT-4, at the protein and mRNA level, was significantly increased in tumor specimens compared with corresponding normal lung tissue (P<0.05). MCT-4 protein expression was significantly associated with depth of invasion (P=0.034). A survival curve analysis indicated that high MCT-4 expression in lung AC was associated with a decreased overall survival rate (P=0.001). Multivariate analysis demonstrated that high MCT-4 level was an independent prognostic factor (hazard ratio, 3.192; 95% confidence interval, 1.804-5.646; P=0.001) for patients with lung AC. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
17921074
Volume :
14
Issue :
5
Database :
Academic Search Index
Journal :
Oncology Letters
Publication Type :
Academic Journal
Accession number :
125520125
Full Text :
https://doi.org/10.3892/ol.2017.6964