Alpha-enolase promotes cell glycolysis, growth, migration, and invasion in non-small cell lung cancer through FAK-mediated PI3K/AKT pathway
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- 作者：Qiao-Fen Fu (1) (2)
Yan Liu (2)
Yue Fan (2)
Sheng-Ni Hua (2)
Hong-Ying Qu (1)
Su-Wei Dong (2)
Rui-Lei Li (4)
Meng-Yang Zhao (1) (2)
Yan Zhen (2)
Xiao-Li Yu (2)
Yi-Yu Chen (1) (2)
Rong-Cheng Luo (1)
Rong Li (1)
Li-Bo Li (1)
Xiao-Jie Deng (1) (2)
Wei-Yi Fang (1) (2)
Zhen Liu (2) (3)
Xin Song (2) (4)
1. Cancer Center ; Traditional Chinese Medicine-Integrated Hospital of Southern Medical University ; Guangzhou ; Guangdong ; People鈥檚 Republic China
2. Cancer Research Institute of Southern Medical University ; Guangzhou ; Guangdong ; People鈥檚 Republic China
4. Department of Cancer Biotherapy Center ; Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province) ; Kunming ; Yunnan ; People鈥檚 Republic China
3. Department of Pathology ; Basic School of Guangzhou Medical University ; Guangzhou ; Guangdong ; People鈥檚 Republic China - 关键词：ENO1 ; NSCLC ; Glycolysis ; Cell proliferation ; FAK/PI3K/AKT ; EMT
- 刊名：Journal of Hematology & Oncology
- 出版年：2015
- 出版时间：December 2015
- 年：2015
- 卷：8
- 期：1
- 全文大小：1,988 KB
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- 出版者：BioMed Central
- ISSN：1756-8722
文摘
Background 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). Methods The 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. Results ENO1 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. Conclusion This study showed that ENO1 is responsible for NSCLC proliferation and metastasis; thus, ENO1 might serve as a potential molecular therapeutic target for NSCLC treatment.