ArticleJournal for immunotherapy of cancer2025
HSP47 inhibition-induced CD155 expression through TRAF2 deubiquitination promotes tumor immune evasion.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHeat shock protein 47 (HSP47) is crucial for protein quality control and tumor progression. While its role in cancer biology is well established, its impact on cancer immunity remains poorly understood. In this study, we aim to elucidate how HSP47 inhibition modulates immune evasion, with a specific focus on the CD155/T-cell immunoreceptor with Ig and ITIM domains (TIGIT) axis in osteosarcoma (OS).
methodsWe used OS cell lines and mouse models to examine the effects of HSP47 inhibition on tumor growth and immune response. Expression levels of CD155, TIGIT, and other immune checkpoint molecules were analyzed throughflow cytometry, immunofluorescence, and western blotting. We also assessed the therapeutic effects of combining HSP47 inhibition with CD155 blockade or nuclear factor-kappa B (NF-κB) inhibitors in preclinical models.
resultsInhibition of HSP47 resulted in increased expression of the immune checkpoint molecule CD155, which impaired the antitumor activity of CD8
conclusionsHSP47 inhibition promotes immune evasion by upregulating CD155 via the TRAF2-NF-κB pathway, which impairs CD8
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