Endoplasmic reticulum stress on glioblastoma: Tumor growth promotion and immunosuppression.

Exogenous or endogenous factors such as hypoxia, nutritional deficiencies, acidic microenvironments and their own high metabolic demands usually lead to tumor endoplasmic reticulum dysfunction and trigger endoplasmic reticulum stress (ERS). ERS sensors intercept such stress signals, which subsequently initiate the unfolded protein response (UPR), enabling tumor cells to adapt robustly in the hostile environment. Many studies have found that the ERS response affects a variety of tumor-infiltrating immune cells and suppresses their anti-tumor responses through different mechanisms. Given that glioblastoma (GBM) are immunosuppressive "cold tumors" with a poor prognosis. This paper not only discusses the promotion of GBM growth by ERS response, but also reviews the mechanisms by which ERS response promotes an immunosuppressive microenvironment.