IGSF9-targeted therapy inhibits the progression of acute myeloid leukemia.

ABSTRACT:

Abstract

Previously, we reported that targeting immunoglobulin superfamily member 9 (IGSF9) could enhance antitumor T-cell activity and sensitivity to anti-PD-1 immunotherapy, although the detailed mechanism remains unclear. In this study, we find that, similar to the regulation of PD-L1 expression, interferon gamma (IFN-γ) also induces the expression of IGSF9 in acute myeloid leukemia (AML). The small interfering RNA specifically targeting JAK1 and a STAT1 inhibitor blocking IFN-γ signal pathway significantly inhibit the expression of IGSF9 and PD-L1. As a tumor-specific immune checkpoint molecule, IGSF9 plays a significant role in promoting tumor escape. The induction of both PD-L1 and IGSF9 by IFN-γ in the tumor microenvironment explains why IGSF9 is highly expressed in tumors a

SUBMITTER: Hui L 

PROVIDER: S-EPMC12362688 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature