High-concentration glucose enhances invasion in invasive ductal breast carcinoma by promoting Glut1/MMP2/MMP9 axis expression

被引:35
作者
Sun, Xian-Fu [1 ]
Shao, Ying-Bo [1 ]
Liu, Ming-Ge [2 ]
Chen, Qi [1 ]
Liu, Zhao-Jun [1 ]
Xu, Bin [1 ]
Luo, Su-Xia [3 ]
Liu, Hui [1 ]
机构
[1] Henan Canc Hosp, Dept Galactophore, 127 Dongming Rd, Zhengzhou 450008, Henan, Peoples R China
[2] Henan Canc Hosp, Dept Pathol, Zhengzhou 450008, Henan, Peoples R China
[3] Henan Canc Hosp, Dept Med Oncol, Zhengzhou 450008, Henan, Peoples R China
关键词
type 2 diabetes mellitus; invasive ductal breast carcinoma; Glut1; MMP2; MMP9; invasion; DIABETES-MELLITUS; LUNG-CANCER; CELL-LINE; RISK;
D O I
10.3892/ol.2017.5843
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Type 2 diabetes mellitus (T2DM) has been considered to he a risk factor for numerous human cancers. Hyperglycemia is one of the most direct internal environmental changes for patients with T2DM. Increasing evidence reveals that a high concentration of glucose can promote tumor progression, while its role for migration and invasion of invasive ductal breast carcinoma (IDBC) cells remains unclear. In the present study, it was demonstrated that IDBC patients with T2DM suffered an increased tumor size and more frequent lymphatic and distant metastasis compared with those without T2DM (P<0.05). MCE-7 breast carcinoma cells, which were cultured in a high glucose concentration medium (25.00 mM), exhibited increased invasion (P<0.05). In addition, the expression of glucose transporters (Gluts), matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9) in IDBC tissues with T2DM was significantly higher compared to those without T2DM. Downregulation of glucose transporter 1 (Glut1) by small interfering RNA may markedly suppress MCF-7 cell invasion as well as the expression of MMP2 and MMP9. These results suggest that T2DM can affect the malignant features of tumors in IDBC. The high glucose concentration in the tumor microenvironment may enhance IDBC invasion via upregulating Glut1/MMP2/MMP9 axis expression.
引用
收藏
页码:2989 / 2995
页数:7
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