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Volume 29, No 1, Jan 2019

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 29 Issue 1, January 2019: 83-86

LETTERS TO THE EDITOR

Palmitoylation stabilizes PD-L1 to promote breast tumor growth

Yi Yang 1, Jung-Mao Hsu 1, Linlin Sun 1,2, Li-Chuan Chan 1,3, Chia-Wei Li 1, Jennifer L. Hsu 1,3, Yongkun Wei 1, Weiya Xia 1,Junwei Hou 1, Yufan Qiu 1,4 and Mien-Chie Hung 1,3

1Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; 2Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 30052, China; 3Graduate School of Biomedical Sciences, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA and 4The 3rd Department of Breast Cancer, China Tianjin Breast Cancer Prevention, Treatment and Research Center, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Tianjin 300060,China
 Correspondence: Mien-Chie Hung (mhung@mdanderson.org)

Dear Editor,

PD-L1 is a well-known transmembrane protein, which is highly expressed on many types of cancer cells. By binding to its receptor PD-1 on T cells, PD-L1 significantly inhibits T cells activation and activity, and thus plays a pivotal role in driving the escape of tumor cells from immune surveillance.1 Antibody blockade of PD-L1/PD-1 interaction has revolutionized cancer therapy with promising clinical outcomes in many cancer types, including melanoma, lung cancer, bladder cancer, colorectal cancer, and renal-cell cancer.2 However, in some others such as prostate cancer, ovarian cancer, and breast cancer, the response rate of PD-L1/PD-1 antibody therapy is less satisfactory.3 Recent studies have shown that PD-L1 can be regulated by post-translational regulations such as ubiquitination,4 phosphorylation and glycosylation,5 providing opportunity for marker-guided effective combinational therapy with immune checkpoint therapy.


https://doi.org/10.1038/s41422-018-0124-5

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