ArticleTranslational oncology2025
Targeting hypoxia-mediated chemo-immuno resistance by a hybrid NBDHEX-Pt(IV) prodrug via declining nuclear STING1-promoted AhR-CIN in human lung squamous cell carcinoma.
Article in Translational oncology, 2025. 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
As found in human lung squamous cell carcinoma (LUSC), STING1 involved in ER-Golgi intermediate compartment (ERGIC) could coordinate immune responses to ectopic DNA triggered by DNA-targeted chemotherapy. ERGIC STING1 is considered to compete with nuclear STING1 to decline aryl hydrocarbon receptor (AhR)-chromosomal instability (CIN)-triggered chronic STING activation which could cause therapeutic resistance. Moreover, GSTP1 was proved to inhibit ERGIC-STING1 via promoting S-glutathione modification of STING1. Hence, a potent GSTP1-targeted Pt(IV) hybrid NBDHEX-DN604, was designed via conjugating a GSTP1 inhibitor NBDHEX to the axial position of Pt(IV) prodrug. As mentioned, hypoxia is mainly observed in malignant tumors and develops acquired drug resistance. In vitro bio-properties of hypoxic SK-MES-1/cDDP cells demonstrated that NBDHEX-DN604 could reverse chemo-immuno resistance via intercepting GSTP1 to activate ERGIC STING1, leading to the decrease of nuclear STING1. The mechanistic data indicated that NBDHEX-DN604 could elevate ERGIC STING1 to mitigate nuclear STING1-mediated AhR-TLS-CIN-chronic activation. Meanwhile, NBDHEX-DN604 was found to decline STING1-AhR-CIN to circumvent chemo-immuno resistance, resulting in predominant in vivo antitumor effect in HY-KLN-205/cDDP-inoculated BALB/c mice. The data provide a novel rationale for the mixed chemo-immunotherapy of NBDHEX-DN604 as a potent Pt(IV) therapeutic method for patients with resistant LUSC.
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