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Title:
Alpha-enolase promotes cell glycolysis, growth, migration, and invasion in non-small cell lung cancer through FAK-mediated PI3K/AKT pathway | Journal of Hematology & Oncology | Full Text
Description:
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.
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eno, cells, cell, nsclc, expression, pubmed, cancer, article, spca, scholar, google, lung, migration, cas, figure, invasion, protein, glycolysis, tissues, levels, central, staining, proliferation, tumor, control, liu, study, enosuppressed, compared, pathway, vitro, growth, significantly, observed, promotes, vivo, mice, results, increased, cmyc, formation, noncancerous, western, stably, treatment, cyclin, china, data, metastasis, overexpressed,
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male balb/c-nu/nu mice springer nature lentivirus-mediated full-length eno1-gfp fak-mediated pi3k/akt pathway fak/pi3k/akt pathway real-time pcr analysis full-length eno1-gfp retinoic acid-mediated therapy epithelial-mesenchymal transition phenotypes inhibits epithelial-mesenchymal transition stained liver sections hypoxia-inducible factor 1alpha stained tissue sections full-length eno1 increased bmc vet res rabbit polyclonal anti-eno1 qiao-fen fu proteasome-dependent protein turnover para-cancer lung tissues transient eno1-suppressed a549 xiao-jie deng received preoperative radiation pi3k/akt pathway conclusions materials sharing eno1-suppressed cells compared giemsa-stained cells adhering eno1-overexpressed cells compared bmc cancer full-length eno1 rui-lei li potential prognostic marker promoting cell glycolysis privacy choices/manage cookies epithelial-mesenchymal transition eno1-suppressed spca-1 cells wei-yi fang human angiotensin ii eno1-suppressed nsclc cells eno1-overexpressed a549 cells authors scientific editing human lung cancer control plv-shctr vector sirna-mediated suppression a549-eno1 cells compared elevated e-cadherin expression glycolysis module activated pten/pi3k/akt cancerous lung specimens
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headline:Alpha-enolase promotes cell glycolysis, growth, migration, and invasion in non-small cell lung cancer through FAK-mediated PI3K/AKT pathway
description: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). 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. 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. 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.
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name:Cancer Research Institute of Southern Medical University, Guangzhou, Peopleās Republic China
name:Cancer Research Institute of Southern Medical University, Guangzhou, Peopleās Republic China
name:Cancer Research Institute of Southern Medical University, Guangzhou, Peopleās Republic China
name:Cancer Research Institute of Southern Medical University, Guangzhou, Peopleās Republic China
name:Cancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Peopleās Republic China
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