ReviewTranslational cancer research2026
Context-dependent roles of HtrA2/Omi in ovarian cancer: mitochondrial apoptotic function linking platinum sensitivity and acquired chemoresistance-a narrative review.
Review in Translational cancer 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
4 authors.
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Abstract
Background and Objective: Epithelial ovarian cancer often responds to platinum therapy but frequently relapses with acquired chemoresistance. HtrA2/Omi is a mitochondrial serine protease that can promote apoptosis after cytosolic release. This narrative review synthesizes ovarian-cancer-specific and mechanistic evidence and asks whether HtrA2/Omi is better understood as a static expression marker or as a stress-activated apoptotic effector linked to platinum response. Methods: PubMed, Web of Science, Scopus, and reference lists were searched through April 30, 2026 and updated through June 25, 2026 using terms related to HtrA2/Omi, PRSS25, ovarian cancer, platinum resistance, apoptosis, X-linked inhibitor of apoptosis protein (XIAP), mitochondrial release, cytosolic release and invasion. A structured narrative approach was used because the ovarian HtrA2/Omi literature is limited, heterogeneous, and unsuitable for pooled quantitative synthesis. Key Content and Findings: This review proposes a two-layer model. Baseline HtrA2/Omi abundance is context dependent and varies with histotype, assay platform, treatment state, and compartment resolution. In contrast, under platinum or mitochondrial stress, cytosolic HtrA2/Omi release more consistently supports XIAP relief, caspase activation, apoptosis, and platinum sensitivity. Persistent post-treatment HtrA2/Omi loss may mark an apoptosis-deficient resistant state. Conclusions: HtrA2/Omi should not be framed as a simple oncogene or tumor suppressor in ovarian cancer. Its clearest value is as a candidate response-linked, compartment-aware marker of platinum-induced apoptotic competence. Clinical use requires longitudinal, histotype-stratified and microenvironment-aware validation before treatment selection.
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