Jianqin Lu

Abstract Eliciting calreticulin (CRT) surface exposure is essential for triggering immunogenic cell death (ICD). However, stanniocalcin 1 (STC1) suppresses CRT translocation by sequestering it within mitochondria, limiting ICD induction in tumours. Here, we show that silencing STC1 enhances CRT surface exposure in Lewis lung carcinoma (LLC) cells when combined with paclitaxel (PTX), converting dying tumour cells into an in-situ vaccine that drives immunoprevention of tumour growth.

Epacadostat (EPA), the most advanced inhibitor targeting the indoleamine 2,3-dioxygenase 1 (IDO1), is a critical endogenous metabolic immune regulator. In preclinical melanoma models [1], EPA potentiated the antitumor efficacy of immune checkpoint blockers (ICB) in comparison to ICB monotherapy. Phase I/II clinical trials proved the excellent safety and significant IDO1 targeting ability of EPA [2].

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