TSPAN32 suppresses chronic myeloid leukemia pathogenesis and progression by stabilizing PTEN.

ABSTRACT: We report herein that TSPAN32 is a key node factor for Philadelphia (Ph⁺) leukemia pathogenesis. We found that TSPAN32 expression was repressed by BCR-ABL and ectopic TSPAN32 expression upon Imatinib treatment inhibited the proliferation of Ph⁺ cell lines. Tspan32 overexpression significantly prevented BCR-ABL induced leukemia progression in a murine model and impaired leukemia stem cell (LSC) proliferation. LSCs represent an obstacle for chronic myeloid leukemia (CML) elimination, which continually replenish leukemia cells and are associated with disease relapse. Therefore, the identification of essential targets that contribute to the survival and self-renewal of LSCs is important for novel curative CML. Mechanistically, TSPAN32 was shown to interact with PTEN, incr

SUBMITTER: Qiu Q 

PROVIDER: S-EPMC9974991 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature