HSP47 inhibition-induced CD155 expression through TRAF2 deubiquitination promotes tumor immune evasion.

ABSTRACT:

Background

Heat 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).

Methods

We 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

SUBMITTER: Mou H 

PROVIDER: S-EPMC12666208 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature