ArticleAmerican journal of translational research2026
LncRNA OTUD6B-AS1 overexpression induces parthanatos in esophageal adenocarcinoma cells by binding to miR-145-5p and promoting AIF expression.
Article in American journal of translational research, 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
objectivesTo investigate the functional role of OTU deubiquitinase 6B-antisense transcript 1 (OTUD6B-AS1) and its potential association with parthanatos - a poly (ADP-ribose) polymerase 1 (PARP-1)/apoptosis-inducing factor (AIF)-mediated regulated cell death pathway - in esophageal adenocarcinoma (EAC), which remains poorly understood.
methodsThe expression patterns of OTUD6B-AS1, miR-145-5p, and its downstream target AIF protein were investigated in EAC cell lines. Gain- and loss-of-function assays were performed
resultOTUD6B-AS1 was reduced significantly, and predominantly localized in the cytoplasm of EAC cells. OTUD6B-AS1 overexpression significantly inhibited EAC cell proliferation, migration, and invasion, and induced cellular apoptosis. Mechanistically, OTUD6B-AS1 functioned as a ceRNA, competitively binging to miR-145-5p and thereby relieving its translational suppression of AIF. This biological pathway promoted parthanatos activation, as evidenced by PARP-1 upregulation, extensive DNA damage (with γ-H2AX deposition), and nuclear translocation of AIF. OTUD6B-AS1-induced antitumor activities were abolished by miR-145-5p overexpression or AIF knockdown. Consistently, OTUD6B-AS1 overexpression substantially suppressed xenograft tumor growth
conclusionOTUD6B-AS1 suppresses EAC progression by sponging miR-145-5p and upregulating AIF to induce parthanatos activation. Targeting this ceRNA regulatory axis may be a therapeutic strategy for EAC.
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