Abstract
This study is to investigate the relationship between ectonucleoside triphosphate diphosphohydrolase 5 (ENTPD5) expression and lung cancer clinicopathological factors, and the impact of ENTPD5 on lung cancer cell functions. Lung cancer specimens and matched adjacent normal tissues were obtained from patients without any preoperative radiotherapy or chemotherapy. Knockdown of ETNPD5 expression led to significantly decreased lung cancer cell growth rate, markedly increased apoptosis and the ability to repair, and significantly reduced invasion. Gene chip tests showed that knockdown of ENTPD5 expression caused more Caspase expression. Quantitative real-time polymerase chain reaction showed that the Caspase 3 expression was significantly increased after the knockdown of ENTPD5. In addition, immunohistochemistry showed that the tumor growth marker, proliferating cell nuclear antigen, was significantly reduced in the knockdown model. Tumorigenicity assay and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay showed that the apoptosis of lung cancer cells was increased in the knockdown model. Our results suggest that ENTPD5 affects lung cancer apoptosis via Caspase 3 pathway, and can be potentially used to monitor prognosis or to guide appropriate therapeutic regimens.
Highlights
Lung cancer, one of the most common malignant tumors, is the leading cause of cancer-related death worldwide [1]
Previous studies highlight the importance of ectonucleoside triphosphate diphosphohydrolase 5 (ENTPD5) that is associated with tumor formation and cancerous progression of prostate cancer cell lines. These findings demonstrate that down-regulation of ENTPD5 expression negatively influences the capacity for tumor cells to survive in adverse conditions
To detect ENTPD5 expression in lung cancer tissues, lung cancer cells were stained for immunohistochemical analysis
Summary
One of the most common malignant tumors, is the leading cause of cancer-related death worldwide [1]. Non-small-cell lung cancer (NSCLC) approximately accounts for 80% of lung cancer cases [2]. Lung cancer is regarded as a kind of genetic disease in which aberrant endogenous pathogenic gene expression contributes to genomic instability that enhances the motility and invasiveness of cancer cells, leading to the characteristics of invasiveness. Despite successful treatment of the primary malignancy, relapse and subsequent distant metastasis still occur in more than one quarter of postoperative patients [3]. Postoperative followups should be performed routinely to search for early metastasis to reduce mortality.
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