Effects of galectin-9 on apoptosis, cell cycle and autophagy in human esophageal adenocarcinoma cells

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Abstract

The incidence of esophageal adenocarcinoma (EAC) is rapidly increasing in western countries. The overall mortality of this disease remains high with a 5-year survival rate of less than 20%, despite remarkable advances in the care of patients with EAC. Galectin-9 (Gal-9) is a tandemrepeat type galectin that exerts anti-proliferative effects on various cancer cell types. The aim of the present study was to evaluate the effects of Gal-9 on human EAC cells and to assess the expression of microRNAs (miRNAs) associated with the antitumor effects of Gal-9 in vitro. Gal-9 suppressed the proliferation of the EAC cell lines OE19, OE33, SK-GT4, and OACM 5.1C. Additionally, Gal-9 treatment induced apoptosis and increased the expression levels of caspase-cleaved cytokeratin 18, activated caspase-3 and activated caspase-9. However, it did not promote cell cycle arrest by reducing cell cycle-related protein levels. Furthermore, Gal-9 increased the level of the angiogenesis-related protein interleukin-8 (IL-8) and markedly altered miRNA expression. Based on these findings, Gal-9 may be of clinical use for the treatment of EAC.

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Akashi, E., Fujihara, S., Morishita, A., Tadokoro, T., Chiyo, T., Fujikawa, K., … Masaki, T. (2017). Effects of galectin-9 on apoptosis, cell cycle and autophagy in human esophageal adenocarcinoma cells. Oncology Reports, 38(1), 506–514. https://doi.org/10.3892/or.2017.5689

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