High Glucose Promotes Epithelial-Mesenchymal Transition of Uterus Endometrial Cancer Cells by Increasing ER/GLUT4-Mediated VEGF Secretion | Zendy

Chunjie Gu | Zendy; Feng Xie | Zendy; Bing Zhang | Zendy; HuiLi Yang | Zendy; Jiao Cheng | Zendy; Yinyan He | Zendy; XiaoYong Zhu | Zendy; DaJin Li | Zendy; MingQing Li | Zendy

Open Access

High Glucose Promotes Epithelial-Mesenchymal Transition of Uterus Endometrial Cancer Cells by Increasing ER/GLUT4-Mediated VEGF Secretion

Author(s) -

Chunjie Gu,

Feng Xie,

Bing Zhang,

HuiLi Yang,

Jiao Cheng,

Yinyan He,

XiaoYong Zhu,

DaJin Li,

MingQing Li

Publication year - 2018

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000494237

Subject(s) - cancer research , estrogen receptor , glut4 , biology , viability assay , gene silencing , epithelial–mesenchymal transition , estrogen , glucose transporter , chemistry , endocrinology , medicine , metastasis , cell , breast cancer , cancer , insulin , biochemistry , gene , genetics

Uterus endometrial cancer (UEC) is the common malignancy among gynecologic cancers, and most of them are type I estrogen-dependent UEC. Diabetes is well-known risk factor for the development of UEC. However, the underlying link between high glucose (HG) and the estrogen receptor in UEC remains unclear. Epithelial-mesenchymal transition (EMT) has also been shown to occur during the initiation of metastasis in cancer progression. The aim of this study was to determine the relationships and roles of HG, estrogen receptor and EMT in the growth and migration of UEC.

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