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Oncol Rep. 2017 Jul;38(1):506-514. doi: 10.3892/or.2017.5689. Epub 2017 Jun 1.

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

Author information

1
Department of Gastroenterology and Neurology, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa 761-0793, Japan.
2
Life Science Research Center, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa 761-0793, Japan.
3
Gastroenterological Surgery, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa 761-0793, Japan.
4
Immunology and Immunopathology, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa 761-0793, Japan.

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 tandem-repeat 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.

PMID:
28586026
DOI:
10.3892/or.2017.5689
[Indexed for MEDLINE]

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