Abstract
BackgroundDuring tumor formation and expansion, increasing glucose metabolism is necessary for unrestricted growth of tumor cells. Expression of key glycolytic enzyme alpha-enolase (ENO1) is controversial and its modulatory mechanisms are still unclear in non-small cell lung cancer (NSCLC).MethodsThe expression of ENO1 was examined in NSCLC and non-cancerous lung tissues, NSCLC cell lines, and immortalized human bronchial epithelial cell (HBE) by quantitative real-time reverse transcription PCR (qRT-PCR), immunohistochemistry, and Western blot, respectively. The effects and modulatory mechanisms of ENO1 on cell glycolysis, growth, migration, invasion, and in vivo tumorigenesis and metastasis in nude mice were also analyzed.ResultsENO1 expression was increased in NSCLC tissues in comparison to non-cancerous lung tissues. Similarly, NSCLC cell lines A549 and SPCA-1 also express higher ENO1 than HBE cell line in both mRNA and protein levels. Overexpressed ENO1 significantly elevated NSCLC cell glycolysis, proliferation, clone formation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo by regulating the expression of glycolysis, cell cycle, and epithelial-mesenchymal transition (EMT)-associated genes. Conversely, ENO1 knockdown reversed these effects. More importantly, our further study revealed that stably upregulated ENO1 activated FAK/PI3K/AKT and its downstream signals to regulate the glycolysis, cell cycle, and EMT-associated genes.ConclusionThis study showed that ENO1 is responsible for NSCLC proliferation and metastasis; thus, ENO1 might serve as a potential molecular therapeutic target for NSCLC treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s13045-015-0117-5) contains supplementary material, which is available to authorized users.
Highlights
Lung cancer arises from the bronchial mucosal epithelium and it is the leading cause of cancer mortality worldwide
Our study showed that ENO1 is overexpressed in non-small cell lung cancer (NSCLC) tissues, and upregulated ENO1 promotes cell glycolysis, proliferation, migration, invasion, and tumorigenicity via the Protein tyrosine kinase 2 (FAK)/Phosphoinositide 3-kinase (PI3K)/V-akt murine thymoma viral oncogene homolog 1 (AKT) pathway
ENO1 is highly expressed in NSCLC Quantitative real-time reverse transcription PCR was used to measure the expression of ENO1 mRNA in 26 fresh primary NSCLC tissues (T), their corresponding para-cancer lung tissues (P), and their corresponding non-cancerous lung tissues (N)
Summary
Lung cancer arises from the bronchial mucosal epithelium and it is the leading cause of cancer mortality worldwide. Non-small cell lung cancer (NSCLC) is the most commonly diagnosed type of lung cancer, accounting for approximately 85% of all cases. The continuous progress has been made for surgical resection, chemotherapy, and During tumor formation and expansion, increasing glucose metabolism is necessary for the unrestricted growth of tumor cells [6]. Distributed in a variety of tissues, αenolase (ENO1) was originally described as an enzyme responsible for the glycolytic pathway [7]. During tumor formation and expansion, increasing glucose metabolism is necessary for unrestricted growth of tumor cells. Expression of key glycolytic enzyme alpha-enolase (ENO1) is controversial and its modulatory mechanisms are still unclear in non-small cell lung cancer (NSCLC)
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