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Activation of endothelial genes for reactive oxygen species (ROS) generation promotes metastasis in a preclinical model

Wednesday, November 06, 2013 — Poster Session I

4:00 p.m. – 6:00 p.m.

FAES Academic Center (Upper-Level Terrace)




  • CK Lee
  • CP Day
  • AM Michalowski
  • M Hollingshead
  • G Merlino


In mouse model of metastasis, early onset is correlated with high expression of NOX4, XDH, and M2 macrophage markers in the metastatic nodules, and HO-1 in neighboring lung tissues. We hypothesize that contact between metastatic tumor cells and blood vessels leads to an increase in reactive oxygen species (ROS) via upregulation of NOX4 and/or XDH in endothelial cells (EC). The host tissue responds by increasing HO-1 expression to reduce ROS and inflammation. To validate our hypothesis, we use Firefly GFP-labeled Lewis Lung Cancer cells (LLC), renila mRPF-labeled Raw264.7 macrophage cells, and 2H11 murine ECs derived from axillary lymph node. In the study, we examined that when LLC are in contact with 2H11, high expression of NOX4, HO-1, MR, and XDH are found. However, when Raw264.7 are present, they seem to down-regulate expression of the same genes. This is in accordance with our hypothesis. Further study is needed to investigate whether anti-oxidant agents can prevent metastasis. We also noted significant difference in gene expression when different concentration of glucose was present in the media. This leads us to believe that the amount of glucose and its product lactate, which can be generated from cancer cells, can regulate gene expression in EC.

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