The long noncoding RNA lnc-EGFR stimulates T-regulatory cells differentiation thus promoting hepatocellular carcinoma immune evasion

Runqiu Jiang, Junwei Tang, Yun Chen, Lei Deng, Jie Ji, Yu Xie, Ke Wang, Wei Jia, Wen-Ming Chu and Beicheng Sun ()
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Runqiu Jiang: Liver Transplantation Center of the First Affiliated Hospital and Collaborative Innovation Center For Cancer Personalized Medicine, Nanjing Medical University
Junwei Tang: Liver Transplantation Center of the First Affiliated Hospital and Collaborative Innovation Center For Cancer Personalized Medicine, Nanjing Medical University
Yun Chen: Nanjing Medical University
Lei Deng: Liver Transplantation Center of the First Affiliated Hospital and Collaborative Innovation Center For Cancer Personalized Medicine, Nanjing Medical University
Jie Ji: Liver Transplantation Center of the First Affiliated Hospital and Collaborative Innovation Center For Cancer Personalized Medicine, Nanjing Medical University
Yu Xie: Liver Transplantation Center of the First Affiliated Hospital and Collaborative Innovation Center For Cancer Personalized Medicine, Nanjing Medical University
Ke Wang: Liver Transplantation Center of the First Affiliated Hospital and Collaborative Innovation Center For Cancer Personalized Medicine, Nanjing Medical University
Wei Jia: Metabolomics Shared Resource, University of Hawaii Cancer Center
Wen-Ming Chu: Cancer Biology Program, University of Hawaii Cancer Center
Beicheng Sun: Liver Transplantation Center of the First Affiliated Hospital and Collaborative Innovation Center For Cancer Personalized Medicine, Nanjing Medical University

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Long noncoding RNAs play a pivotal role in T-helper cell development but little is known about their roles in Treg differentiation and functions during the progression of hepatocellular carcinoma (HCC). Here, we show that lnc-epidermal growth factor receptor (EGFR) upregulation in Tregs correlates positively with the tumour size and expression of EGFR/Foxp3, but negatively with IFN-γ expression in patients and xenografted mouse models. Lnc-EGFR stimulates Treg differentiation, suppresses CTL activity and promotes HCC growth in an EGFR-dependent manner. Mechanistically, lnc-EGFR specifically binds to EGFR and blocks its interaction with and ubiquitination by c-CBL, stabilizing it and augmenting activation of itself and its downstream AP-1/NF-AT1 axis, which in turn elicits EGFR expression. Lnc-EGFR links an immunosuppressive state to cancer by promoting Treg cell differentiation, thus offering a potential therapeutic target for HCC.

Date: 2017
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DOI: 10.1038/ncomms15129

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