ArticleOncogene2026
Therapeutic optimization of LIPA targeting to induce endoplasmic reticulum stress and cell death in ovarian cancer.
Article in Oncogene, 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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35 authors.
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Abstract
Ovarian cancer (OCa) remains the most lethal gynecologic malignancy in the United States, with a five-year survival rate below 20%. Elevated basal levels of endoplasmic reticulum stress (ERS) have recently emerged as a therapeutic vulnerability in OCa. We have previously shown that the tris-benzamide ERX-41 can induce ERS and cancer cell death in OCa by targeting LIPA. In this study, using iterative structure-activity relationship-guided studies to enhance activity in OCa, we identified a more potent ERX-41-derived analog, ERX-208. Importantly, ERX-208 consistently and significantly reduced cell viability in 23 OCa cell lines spanning five major histological OCa subtypes, with IC₅₀ values ranging from 50-100 nM, compared to ∼500 nM for ERX-41. Notably, ERX-208 showed minimal cytotoxicity toward normal ovarian surface epithelial cells, indicating cancer cell selectivity. ERX-208 induced apoptosis and suppressed colony formation in vitro in OCa cells. Mechanistic studies using RNA sequencing, Western blotting, RT-qPCR, transmission electron microscopy, and immunohistochemistry validated robust activation of ERS pathways upon ERX-208 treatment. Through in silico molecular docking simulation and confirmatory detailed site-directed mutagenesis, we identified that ERX-208 binds to LIPA over a broader interaction surface than ERX-41. At the 10 mg/kg dose, ERX-208 demonstrated favorable biodistribution, no observable toxicity, and potent antitumor efficacy in vivo against established cell line-derived xenograft (CDX), patient-derived xenograft (PDX), and patient-derived explant (PDE) models. Immunohistochemical analysis of treated tumors demonstrated changes in expression of proliferative marker (ki67, decreased) and the ERS marker (GRP78, increased). These findings support the clinical advancement of ERX-208 for the treatment of patients with OCa.
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