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MTSS1 Curtails Lung Adenocarcinoma Immune Evasion by Promoting AIP4-Mediated PD-L1 Monoubiquitination and Lysosomal Degradation

PD-L1/PD-1 immune therapy for the treatment of cancer has shown tremendous promise; however, there are growing examples of poor response and drug resistance. Many studies have been performed to better understand how PD-L1 is regulated at the genetic, transcription, and translational levels. Recent data by Wang et al. identified a mechanism by which monoubiquitination of PD-L1 via MTSS1/AIP4 dependent mechanisms is critical for PD-L1 expression and lung adenocarcinoma immune evasion. Utilizing immune-compromised mouse models, the group showed that MTSS1 suppressed lung adenocarcinoma progression in a host-immunity-dependent fashion.

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Above: Schematic showing the mechanism by which EGFR/Ras signaling can suppress MTSS1 as a mechanism to control PD-L1 monoubiquitination and its lysosomal degradation to control immune surveillance. 

Link to Citation:

Wang Y. et al. MTSS1 curtails lung adenocarcinoma immune evasion by promoting AIP4-mediated PD-L1 monoubiquitination and lysosomal degradation. Cell Discov. 2023 Feb 21;9(1):20. doi: 10.1038/s41421-022-00507-x.

Supporting Citations

Horita H et al. Identifying Regulatory Posttranslational Modifications of PD-L1: A Focus on Monoubiquitination. Neoplasia. 2017 Apr;19(4):346-353. doi: 10.1016/j.neo.2017.02.006.

Middleton-Davis F et al. Method for detecting acetylated PD-L1 in cell lysates by immunoprecipitation and western blot analysis. PLoS One. 2022 Jul 18;17(7):e0268887. doi: 10.1371/journal.pone.0268887.

Related Product Used:

Signal-Seeker™ Ubiquitination Detection Kit (Cat # BK161)

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