@article{APS10487,
author = {Fei-fei Xu and Hui-min Sun and Run-ping Fang and Lu Zhang and Hui Shi and Xue Wang and Xue-li Fu and Xian-meng Li and Xu-he Shi and Yue Wu and Kai Ye and Wei-ying Zhang and Li-hong Ye},
title = {The modulation of PD-L1 induced by the oncogenic HBXIP for breast cancer growth},
journal = {Acta Pharmacologica Sinica},
volume = {43},
number = {2},
year = {2022},
keywords = {},
abstract = {Programmed death ligand-1 (PD-L1)/PD-1 checkpoint extensively serves as a central mediator of immunosuppression. A tumor- promoting role for abundant PD-L1 in several cancers is revealed. However, the importance of PD-L1 and how the PD-L1 expression is controlled in breast cancer remains obscure. Here, the mechanisms of controlling PD-L1 at the transcription and protein acetylation levels in promoting breast cancer growth are presented. Overexpressed PD-L1 accelerates breast cancer growth in vitro and in vivo. RNA-seq uncovers that PD-L1 can induce some target genes affecting many cellular processes, especially cancer development. In clinical breast cancer tissues and cells, PD-L1 and HBXIP are both increased, and their expressions are positively correlated. Mechanistic exploration identifies that HBXIP stimulates the transcription of PD-L1 through co-activating ETS2. Specifically, HBXIP induces PD-L1 acetylation at K270 site through interacting with acetyltransferase p300, leading to the stability of PD-L1 protein. Functionally, depletion of HBXIP attenuates PD-L1-accelerated breast tumor growth. Aspirin alleviates breast cancer via targeting PD-L1 and HBXIP. Collectively, the findings display new light into the mechanisms of controlling tumor PD-L1 and broaden the utility for PD-L1 as a target in breast cancer therapy.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/10487}
}