Supplementary material from "miR-149-3p reverses CD8+ T-cell exhaustion by reducing inhibitory receptors and promoting cytokine secretion in breast cancer cells"
Posted on 2019-09-24 - 12:11
Blockade of inhibitory receptors (IRs) is one of the most effective immunotherapeutic approaches to treat cancer. Dysfunction of miRNAs is a major cause of aberrant expression of IRs and contributes to the immune escape of cancer cells. How miRNAs regulate immune checkpoint proteins in breast cancer remains largely unknown. In this study, downregulation of miRNAs was observed in PD-1-overexpressing CD8+ T cells using miRNA array analysis of mouse breast cancer homografts. The data reveal that miR-149-3p was predicted to bind the 3'UTRs of mRNAs encoding T-cell inhibitor receptors PD-1, TIM-3, BTLA and Foxp1. Treatment of CD8+ T cells with an miR-149-3p mimic reduced apoptosis, attenuated changes in mRNA markers of T-cell exhaustion and downregulated mRNAs encoding PD-1, TIM-3, BTLA and Foxp1. On the other hand, T-cell proliferation and secretion of effector cytokines indicative of increased T-cell activation (IL-2, TNF-α, IFN-γ) were upregulated after miR-149-3p mimic treatment. Moreover, the treatment with a miR-149-3p mimic promoted the capacity of CD8+ T cells to kill targeted 4T1 mouse breast tumour cells. Collectively, these data show that miR-149-3p can reverse CD8+ T-cell exhaustion and reveal it to be a potential antitumour immunotherapeutic agent in breast cancer.
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Zhang, Meng; Gao, Dian; Shi, Yanmei; Wang, Yifan; Joshi, Rakesh; Yu, Qiongfang; et al. (2019). Supplementary material from "miR-149-3p reverses CD8+ T-cell exhaustion by reducing inhibitory receptors and promoting cytokine secretion in breast cancer cells". The Royal Society. Collection. https://doi.org/10.6084/m9.figshare.c.4676036.v1
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AUTHORS (14)
MZ
Meng Zhang
DG
Dian Gao
YS
Yanmei Shi
YW
Yifan Wang
RJ
Rakesh Joshi
QY
Qiongfang Yu
DL
Daheng Liu
FA
Faizah Alotaibi
YZ
Yujuan Zhang
HW
Hongmei Wang
QL
Qing Li
ZZ
Zhu-Xu Zhang
JK
James Koropatnick
WM
Weiping Min