Blood: Mitochondrial vector homologous gene MTCH2 is essential for AML survival

Center point:inhibition of MTCH2 can increase the levels of acetone acid and PDH in the nucleus, resulting in AML differentiation and loss of transplant potentialthis study defines a new mechanism for mitochondrial pathways to regulate aML epigenetics and differentiationSummary:in order to identify the mitochondrial genes needed for the growth of AML (acute myeloid leukemia) cells, the researchers used CRISPR technology to screen and identify the mitochondrial in vitro membrane protein MTCH2 (mitochondrial carrier homologous 2)In AML cells, knocking down the expression of MTCH2 inhibits cell growth, reduces the transplant potential of stem cells and induces the cell differentiation processInhibiting the expression of MTCH2 in AML cells can increase the expression level of acetone acid and acetone dehydrogenase in the nucleus, thereby inducing acetylation of histones and promoting differentiation of AML cells, the study found that inhibiting MTCH2 expression increased the levels of acetone acid and PDH in the nucleus, which in turn led to the differentiation of AML and the loss of transplant potential, revealing new mechanisms for mitochondrial pathways to regulate AML epigenetics and stem cell differentiation