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.
 W. Bernard, P. Stewart Christopher, World Cancer Report 2014, International Agency for Research on Cancer, WHO, 2014.  J. Ferlay, I. Soerjomataram, M. Ervik, R. Dikshit, S. Eser, C. Mathers, et al., GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase, IARC, 2013.  L.A. Raedler, Lonsurf (trifluridine plus tipiracil): a new oral treatment approved for patients with metastatic colorectal cancer, Am. Health Drug Benefits 9 (2016)
 R. Wang, P.S. Billone, W.M. Mullett, Nanomedicine in action: an overview of cancer
 S.Y. Han, B.H. You, Y.C. Kim, Y.W. Chin, Y.H. Choi, Dose-independent ADME properties and tentative identification of metabolites of α-mangostin from Garcinia mangostana in mice by automated microsampling and UPLC-MS/MS methods, PLoS One 10 (7) (2015) e0131587.
 W. Samprasit, P. Akkaramongkolporn, S. Jaewjira, P. Opanasopit, Design of alpha mangostin-loaded chitosan/alginate controlled-release nanoparticles using genipin as crosslinker, J. Drug Deliv. Sci. Technol. 46 (2018) 312–321.  A.A. Elsaid Ali, M. Taher, F. Mohamed, Microencapsulation of alpha-mangostin into PLGA microspheres and optimization using response surface methodology intended for pulmonary delivery, J. Microencapsul. 30 (8) (2013) 728–740.
 S. Jamzad, R. Fassihi, Role of surfactant and MIK665 (S-64315) on dissolution properties of feno-fibrate and glipizide-a technical note, AAPS PharmSciTech 7 (2) (2006) E33.
L. Peltonen, T. Laaksonen, Dissolution studies of poorly soluble drug nanosuspen-sions in non-sink conditions, AAPS PharmSciTech 14 (2) (2013) 748–756.  J. Israelachvili, Intermolecular & Surface Forces, third ed., London Academic Press, USA, 1985.  S.A. Macpherson, G.B. Webber, R. Moreno-Atanasio, Aggregation of nanoparticles in high ionic strength suspensions: eﬀect of Hamaker constant and particle con-centration, Adv. Powder Technol. 23 (4) (2012) 478–484.
 R. Benjakul, L. Kongkaneramit, N. Sarisuta, P. Moongkarndi, C.C. Müller-Goymann, Cytotoxic eﬀect and mechanism inducing cell death of α-mangostin liposomes in various human carcinoma and normal cells, Anticancer Drugs 26 (8) (2015)
Contents lists available at ScienceDirect
European Journal of Pharmacology
journal homepage: www.elsevier.com/locate/ejphar
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
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.