Abstract

Endometrial cancer is the most common gynecologic malignancy and is associated with increased morbidity each year, including young people. However, its mechanisms of proliferation and progression are not fully elucidated. It is well known that abnormal glycosylation is involved in oncogenesis, and fucosylation is one of the most important types of glycosylation. In particular, fucosyltransferase 8 (FUT8) is the only FUT responsible for α1, 6-linked fucosylation (core fucosylation), and it is involved in various physiological as well as pathophysiological processes, including cancer biology. Therefore, we aimed to identify the expression of FUT8 in endometrial endometrioid carcinoma and investigate the effect of the partial silencing of the FUT8 gene on the cell proliferation of Ishikawa cells, an epithelial-like endometrial cancer cell line. Quantitative real-time PCR analysis showed that FUT8 gene expression was significantly elevated in the endometrial endometrioid carcinoma, compared to the normal endometrium. The immunostaining of FUT8 and Ulex europaeus Agglutinin 1 (UEA-1), a kind of lectin family specifically binding to fucose, was detected endometrial endometrioid carcinoma. The proliferation assay showed FUT8 partial knockdown by transfection of siRNA significantly suppressed the proliferation of Ishikawa cells, concomitant with the upregulation in the gene expressions associated with the interesting pathways associated with de-ubiquitination, aspirin trigger, mesenchymal-epithelial transition (MET) et al. It was suggested that the core fucosylation brought about by FUT8 might be involved in the proliferation of endometrial endometrioid carcinoma cells.

Highlights

  • Endometrial cancer is one of the most common gynecologic malignancies

  • fucosyltransferase 8 (FUT8) gene expression was elevated in the tissues of endometrial endometrioid carcinoma

  • The gene expression of FUT7 and FUT8 was significantly increased in endometrial endometrioid carcinoma tissues, compared to those of the normal endometrium (P < 0.05, Fig. 1F and Fig. 1G)

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Summary

Introduction

Endometrial cancer is one of the most common gynecologic malignancies. In the United States, there were an estimated 54,870 newly diagnosed cases and 10,170 deaths in 2016 [1]. The associated morbidity, including among young people, increases each year. Endometrial endometrioid carcinoma is the most common histologic type of endometrial cancer and comprises 80% of all cases [2,3]. The main risk factor for endometrial endometrioid carcinoma is long-term exposure to excess endogenous or exogenous estrogen without adequate opposition by a progestin [4]. Its mechanism of proliferation is not fully elucidated; in particular

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