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ROS release by PPARβ/δ-null fibroblasts reduces tumor load through epithelial antioxidant response.

Abstract：

:Tumor stroma has an active role in the initiation, growth, and propagation of many tumor types by secreting growth factors and modulating redox status of the microenvironment. Although PPARβ/δ in fibroblasts was shown to modulate oxidative stress in the wound microenvironment, there has been no evidence of a similar effect in the tumor stroma. Here, we present evidence of oxidative stress modulation by intestinal stromal PPARβ/δ, using a FSPCre-Pparb/d-/- mouse model and validated it with immortalized cell lines. The FSPCre-Pparb/d-/- mice developed fewer intestinal polyps and survived longer when compared with Pparb/dfl/fl mice. The pre-treatment of FSPCre-Pparb/d-/- and Pparb/dfl/fl with antioxidant N-acetyl-cysteine prior DSS-induced tumorigenesis resulted in lower tumor load. Gene expression analyses implicated an altered oxidative stress processes. Indeed, the FSPCre-Pparb/d-/- intestinal tumors have reduced oxidative stress than Pparb/dfl/fl tumors. Similarly, the colorectal cancer cells and human colon epithelial cells also experienced lower oxidative stress when co-cultured with fibroblasts depleted of PPARβ/δ expression. Therefore, our results establish a role for fibroblast PPARβ/δ in epithelial-mesenchymal communication for ROS homeostasis.

journal_name

Oncogene

journal_title

Oncogene

authors

Tan EHP,Sng MK,How ISB,Chan JSK,Chen J,Tan CK,Wahli W,Tan NS

doi

10.1038/s41388-017-0109-8

subject

Has Abstract

pub_date

2018-04-01 00:00:00

pages

2067-2078

issue

15

eissn

0950-9232

issn

1476-5594

pii

10.1038/s41388-017-0109-8

journal_volume

37

pub_type

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