ArticleCancer immunology, immunotherapy : CII2026
HMGB1 ubiquitination inhibition and extracellular secretion, mediated by m
Article in Cancer immunology, immunotherapy : CII, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMALAT1 has been validated to favor the progression of acute lymphoblastic leukemia (ALL), but its detailed mechanism remains obscure. This study explored the functional roles of ALL cells-derived exosomal MALAT1 in chemoresistance and malignant growth of ALL cells, as well as its underlying mechanisms.
methodsThe expression of target molecules was evaluated by qRT-PCR, Western blotting, immunofluorescence, and immunohistochemical staining. CCK-8, EdU staining and flow cytometry were conducted to determine cell proliferation and apoptosis. RIP, RNA-pull down, Co-IP, and MeRIP were used to investigate molecular mechanisms. ALL cells were injected into nude mice to evaluate in vivo tumor formation.
resultsMALAT1 and methyltransferase-like 14 (METTL14) were up-regulated in ALL, which exhibited a positive correlation. METTL14-mediated m
conclusionALL cells-derived exosomal MALAT1 was up-regulated by METTL14-mediated m HIGHLIGHTS: (1) METTL14 and MALAT1 were positively correlated in ALL samples. (2) METTL14 increased MALAT1 stability and expression in an IGF2BP1-mediated m6A manner. (3) ALL cells transferring exosomal MALAT1 suppressed TRIM27-mediated HMGB1 ubiquitination in NK92-MI cells. (4) HMGB1 silencing in NK92-MI cells enhanced adriamycin sensitivity of ALL cells. (5) MALAT1/HMGB1 axis inhibition delayed in vivo ALL growth via NK cell activation.
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