2. Academic Validation
  3. Ubiquitin C-terminal hydrolase L1 promotes expression of programmed cell death-ligand 1 in non-small-cell lung cancer cells

Ubiquitin C-terminal hydrolase L1 promotes expression of programmed cell death-ligand 1 in non-small-cell lung cancer cells

  • Cancer Sci. 2020 Sep;111(9):3174-3183. doi: 10.1111/cas.14529.
Rudi Mao 1,  Xiao Tan 2,  Ying Xiao 3,  Xinyu Wang 1,  Zhixing Wei 1,  Jianing Wang 1,  Xiaoyan Wang 1,  Huaiyu Zhou 4,  Lining Zhang 1,  Yongyu Shi 1
Affiliations

Affiliations

  • 1 Department of Immunology and Shandong Key Laboratory of Infection and Immunity, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, China.
  • 2 Department of Pathology, Linyi People's Hospital, Linyi, China.
  • 3 Molecular Medicine Experimental Teaching Platform, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, China.
  • 4 Department of Parasitology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, China.
PMID: 32539182 DOI: 10.1111/cas.14529
Abstract

Programmed cell death-ligand 1 (PD-L1) expressed on Cancer cells can cause immune escape of non-small-cell lung Cancer (NSCLC). Elucidation of the regulatory mechanisms of the PD-L1 expression is a prerequisite for establishing new tumor immunotherapy strategies. Ubiquitin C-terminal hydrolase L1 (UCHL1) is a regulator of cellular signaling transduction that is aberrantly expressed in NSCLC. However, it is not known whether UCHL1 regulates the expression of PD-L1 in NSCLC cells. In the present study, we found that UCHL1 promotes the expression of PD-L1 in NSCLC cell lines. In addition, UCHL1 expressed in NSCLC cells inhibited activation of Jurkat cells through upregulation of PD-L1 expression in in vitro experiments. Moreover, UCHL1 upregulates PD-L1 expression through facilitating activation of the AKT-P65 signaling pathway. In conclusion, these results indicated that UCHL1 promoted PD-L1 expression in NSCLC cells. This finding implied that inhibition of UCHL1 might suppress immune escape of NSCLC through downregulation of PD-L1 expression in NSCLC cells.

Keywords

AKT; NSCLC; P65; PD-L1; UCHL1.

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