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2016 ; 291
(40
): 21085-21095
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Amphiregulin Confers Regulatory T Cell Suppressive Function and Tumor Invasion
via the EGFR/GSK-3?/Foxp3 Axis
#MMPMID27432879
Wang S
; Zhang Y
; Wang Y
; Ye P
; Li J
; Li H
; Ding Q
; Xia J
J Biol Chem
2016[Sep]; 291
(40
): 21085-21095
PMID27432879
show ga
Previous studies mainly focused on the role of the epidermal growth factor
receptor (EGFR) in tumor cells, whereas the effects of the EGFR on immune
responses has not been determined. Our study shows that the EGFR signaling
pathway play a role in the regulation of regulatory T cells (Treg cells) in
cancer patients. The EGF-like growth factor Amphiregulin (AREG) protein was
frequently up-regulated in a tissue microarray, which was associated with worse
overall survival. Additionally, in sera, tissue specimens, and effusions of lung
or gastric cancer patients, up-regulated AREG protein enhanced the suppressive
function of Treg cells. AREG maintained the Treg cell suppressive function via
the EGFR/GSK-3?/Foxp3 axis in vitro and in vivo Furthermore, inhibition of EGFR
by the tyrosine kinase inhibitor gefitinib restored the activity of GSK-3? and
attenuated Treg cell function. ?-TrCP was involved in GSK-3?-mediated Foxp3
degradation, and mass spectrometry identified Lys(356) as the ubiquitination site
of Foxp3 by ?-TrCP. These findings demonstrate the posttranslational regulation
of Foxp3 expression by AREG in cancer patients through AREG/EGFR/GSK-3?
signaling, which could lead to Foxp3 protein degradation in Treg cells and a
potential therapeutic target for cancer treatment.
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