• 2019-10
  • 2020-03
  • 2020-07
  • 2020-08
  • br Acknowledgements br This work


    This work was supported by the Thailand Research Fund (TRF) under the Royal Golden Jubilee (RGJ) Ph.D. Grant No. PHD/0234/2560 RGJ and the Naresuan University Grant No. R2561B009. Duy Toan Pham sincerely thanks Naresuan University ASEAN Scholarship, the RGJ Ph.D. Grant, the Boosting Research Potential of Naresuan University Students program, Batch 4, and the Naresuan University Scholarship for Oral Presentation for financial support. Special thanks to Ms. Tashatai Prasertpol and Ms. Piangpetch Tanngoen for the ana-lytical data. Many thanks to Mr. Peter Barton of the NULC Writing Clinic, Naresuan University, for his English editing. Finally, thank you, mom and dad, for everything.
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    Contents lists available at ScienceDirect
    European Journal of Pharmacology
    journal homepage:
    Molecular and cellular pharmacology
    Alpha-enolase promotes gastric cancer cell proliferation and metastasis via T regulating AKT signaling pathway
    Liang Suna,1, Ting Lub,1, Kangjun Tiana, Diyuan Zhoua, Jingfeng Yuana, Xuchao Wanga, Zheng Zhua, Daiwei Wana, Yizhou Yaoa, Xinguo Zhua, , Songbing Hea, a Department of General Surgery, the First Affiliated Hospital of Soochow University, Suzhou 215006, China
    b Department of Gastroenterology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China
    Cancer metabolism
    Gastric cancer 
    Increased aerobic glycolysis is considered as a hallmark of cancer and targeting key glycolytic enzymes will be a promising therapeutic approach in cancer treatment. Alpha-enolase (ENO1), as a prominent glycolytic enzyme, is upregulated in multiple cancers and its overexpression is involved in tumor cell proliferation and metastasis. In the present study, we aimed to investigate the potential role of ENO1 in the development and progression of gastric cancer (GC). Here, we found that ENO1 expression was upregulated in human GC and was associated with Lauren type, lymph node metastasis (LNM) and TNM stage. Knockdown of ENO1 attenuated GC cell proliferation and metastasis and reversed epithelial-mesenchymal transition (EMT) progress in vitro while ENO1 overexpression did the opposite. ENO1 could modulate AKT signaling pathway in GC cells and the enhanced proliferation and migration ability induced by ENO1 overexpression was impaired after incubation with PI3K inhibitor Ly294002 in SGC7901 cells. Our data demonstrated that ENO1 enhances GC cell proliferation and metastasis through the protein kinase B (AKT) signaling pathway, indicating that ENO1/AKT signaling axis may serve as a potential target for treatment of GC.