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Article Abstract
Acute myeloid leukemia (AML) with a () mutation is a unique subtype of adult leukemia. Recent studies show that -mutated AML has high autophagy activity. However, the mechanism for upholding the high autophagic level is still not fully elucidated. In this study, we first identified that tumor protein p53 inducible nuclear protein 2 (TP53INP2) was highly expressed and cytoplasmically localized in -mutated AML cells. Subsequent data showed that the expression of TP53INP2 was upregulated by fat mass and obesity-associated protein (FTO)-mediated mA modification. Meanwhile, TP53INP2 was delocalized to the cytoplasm by interacting with NPM1 mutants. Functionally, cytoplasmic TP53INP2 enhanced autophagy activity by promoting the interaction of microtubule-associated protein 1 light chain 3 (LC3) - autophagy-related 7 (ATG7) and further facilitated the survival of leukemia cells. Taken together, our study indicates that TP53INP2 plays an oncogenic role in maintaining the high autophagy activity of -mutated AML and provides further insight into autophagy-targeted therapy of this leukemia subtype.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9865930 | PMC |
| http://dx.doi.org/10.3390/ijms24021624 | DOI Listing |
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