Overexpression of GLUT3 promotes metastasis of triple-negative breast cancer by modulating the inflammatory tumor microenvironment

doi:10.1002/jcp.30189

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標題:	Overexpression of GLUT3 promotes metastasis of triple-negative breast cancer by modulating the inflammatory tumor microenvironment
作者:	Tsai, Tai-Hua Yang, Ching-Chieh Kou, Tai-Chih Yang, Chang-En Dai, Jia-Zih Chen, Chia-Ling Lin, Cheng-Wei
貢獻者:	Taipei Med Univ, Coll Med, Sch Med, Dept Biochem & Mol Cell Biol Taipei Med Univ, Grad Inst Med Sci, Coll Med Chi Mei Med Ctr, Dept Radiat Oncol Chia Nan Univ Pharm & Sci, Dept Pharm Taipei Med Univ, Sch Resp Therapy Taipei Med Univ, Wan Fang Hosp, Cell Physiol & Mol Image Res Ctr Kaohsiung Med Univ, Drug Dev & Value Creat Res Ctr
關鍵字:	glycolysis inflammation triple-negative breast cancer tumor microenvironment tumor-associated macrophage
日期:	2021
上傳時間:	2023-11-11 11:59:20 (UTC+8)
出版者:	WILEY
摘要:	Triple-negative breast cancer (TNBC) exhibits a higher level of glycolytic capacity and are commonly associated with an inflammatory microenvironment, but the regulatory mechanism and metabolic crosstalk between the tumor and tumor microenvironment (TME) are largely unresolved. Here, we show that glucose transporter 3 (GLUT3) is particularly elevated in TNBC and associated with metastatic progression and poor prognosis in breast cancer patients. Expression of GLUT3 is crucial for promoting the epithelial-to-mesenchymal transition and enhancing invasiveness and distant metastasis of TNBC cells. Notably, GLUT3 is correlated with inflammatory gene expressions and is associated with M1 tumor-associated macrophages (TAMs), at least in part by C-X-C Motif Chemokine Ligand 8 (CXCL8). We found that expression of GLUT3 regulates CXCL8 production in TNBC cells. Secretion of CXCL8 participates in GLUT3-overexpressing TNBC cells-elicited activation of inflammatory TAMs, which further enhances GLUT3 expression and mobility of TNBC cells. Our findings demonstrate that aerobic glycolysis in TNBC not only promotes aggressiveness of tumor cells but also initiates a positive regulatory loop for enhancing tumor progression by modulating the inflammatory TME.
關聯:	J CELL PHYSIOL, v.236, n.6, pp.4669-4680
顯示於類別:	[藥學系(所)] 期刊論文

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