Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster Display session 1

2287 - Aberrant glycolysis associates with inflammatory tumor microenvironment and promotes metastasis in triple-negative breast cancer


28 Sep 2019


Poster Display session 1


Basic Science

Tumour Site

Breast Cancer


Chengwei Lin


Annals of Oncology (2019) 30 (suppl_5): v1-v24. 10.1093/annonc/mdz238


C. Lin

Author affiliations

  • Department Of Biochemistry And Molecular Cell Biology, Taipei Medical University, 11031 - Taipei City/TW


Login to get immediate access to this content.

If you do not have an ESMO account, please create one for free.

Abstract 2287


Triple-negative breast cancer (TNBC) is account for 10∼25% of breast cancer incidence with more aggressive phenotype, metastatic capability, and poorer prognosis than other subtypes. Altered cancer metabolism is an emerging hallmark of cancer. Previous studies reported that TNBC cells exhibit greater aerobic glycolysis than non-TNBC cells; however, the detailed regulatory mechanism is largely unknown.


The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to analyze expression of glycolytic genes and clinical relevance in TNBC patients. Immunohistochemistry assay was performed to confirm the expression of glycolytic gene in breast cancer tissues. Gain-of-function and loss-of-function studies were conducted in TNBC cell lines. The effect of inflammatory microenvironment was carried out by coculture of macrophages and TNBC cells, and the expression of inflammatory cytokines were performed by real-time PCR.


We compared the differential genes expression in TNBC and non-TNBC by in silico analysis. Interestingly, the expression of glucose transporter 3 (Glut3) is upregulated in TNBC patients, compared to non-TNBC patients. Mechanistically, overexpression of Glut3 regulated the expression of epithelial-mesenchymal transition (EMT) genes and promoted invasiveness and metastasis of TNBC cells. Activation of IL6/STAT3 signaling regulates the expression of Glut3 and glycolytic genes, and coexpression of IL6/Glut3 rendered poorer survival outcome, particularly in TNBC. Moreover, conditioned medium (CM) from Glut3-expressing tumor cells induced macrophage activation and production of pro-inflammatory cytokines, and patients with high Glut3 level associated with inflammaotry signautres.


Upregulation of IL6/STAT3 signaling axis promotes expression of Glut3 and glycolytic genes. Elevation of Glut3 in TNBC induces macrophage activation and production of pro-inflammatory cytokines. Our data show the possible association between glucose metabolism and inflammatory microenvironment in TNBC.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The author.


Ministry of Science and Technology, Taiwan.


The author has declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.