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Kong, Tim; Ahn, Ryuhjin; Yang, Kangning; Zhu, Xianbing; Fu, Zheng; Morin, Geneviève; Bramley, Rachel; Cliffe, Nikki C; Xue, Yibo; Kuasne, Hellen; Li, Qinghao; Jung, Sungmi; Gonzalez, Anne V; Camilleri-Broet, Sophie; Guiot, Marie-Christine; Park, Morag; Ursini-Siegel, Josie; Huang, Sidong
Cancer research, 2020-Feb-01, 2020-02-01, 20200201, Letnik: 80, Številka: 3Journal Article
The PD-L1 (CD274) immune-checkpoint ligand is often upregulated in cancers to inhibit T cells and elicit immunosuppression. Independent of this activity, PD-L1 has recently been shown to also exert a cancer cell-intrinsic function promoting tumorigenesis. Here, we establish this tumor-intrinsic role of PD-L1 in triple-negative breast cancer (TNBC) and non-small cell lung cancer (NSCLC). Using FACS-assisted shRNA screens, we identified the cell-surface adhesion receptor CD44 as a key positive regulator of PD-L1 expression in these cancers. Mechanistically, CD44 activated transcription in part through its cleaved intracytoplasmic domain (ICD), which bound to a regulatory region of the locus containing a consensus CD44-ICD binding site. Supporting this genetic interaction, CD44 positively correlated with PD-L1 expression at the mRNA and protein levels in primary tumor samples of TNBC and NSCLC patients. These data provide a novel basis for CD44 as a critical therapeutic target to suppress PD-L1 tumor-intrinsic function. SIGNIFICANCE: CD44 is a potential target to suppress PD-L1 function in TNBC. This finding has the potential to open a new area of therapy for TNBC.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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