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Study on the mechanism of toll-like receptor junction molecule TICAM1 promoting the occurrence and development of acute myeloid leukemia

ABSTRACT: TICAM1 is recruited into intracellular vesicles to mediate TLR3/4 signaling involved in innate immunity, however the role of this pathway in the pathogenesis of acute myeloid leukemia (AML) remains unknown. We found that in myelomonocytic (M4) and monocytic (M5) AML cells, TLR3/4 was highly expressed, and activation of TLR3/4-TICAM1 signaling was an independent indicator of poor prognosis. TLR3/4 agonists significantly promoted the proliferation of these subtypes of AML cells but inhibited the proliferation of other subtypes of AML cells. Silencing TICAM1 significantly inhibited the growth of M5 AML cells in vitro and in vivo, enhanced their chemotherapy sensitivity, and led to decreased phosphorylation of TBK1 and RIPK3. Using MLL-AF9-driven murine AML model, we investigated the molecular mechanism by which TLR3/4-TICAM1 signaling promotes AML cell growth and drug resistance in vivo and in vitro. Therefore, this study likely provides a new theoretical and experimental basis for the treatment of such disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE270403 | GEO | 2026/03/17

REPOSITORIES: GEO

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Study on the mechanism of toll-like receptor junction molecule TICAM1 promoting the occurrence and development of acute myeloid leukemia

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