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Lung Neoplasms / Cell Line, Tumor / Carcinoma, Non Small Cell Lung · Journal article
Cancer Biology & Therapy · July 20, 2026
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Bis-(di-4-phenyl-benzylaminethiocarbonyl)disulfide reverses cisplatin resistance in A549 NSCLC cells overexpressing ABCC2 and ALDH3A1 via inhibition of these proteins, but not in NCI-H158 cells. Patient data identified a subgroup with Z-score >1.5 for ABCC2 and ALDH3A1 overexpression who may benefit from this combination approach.
In vitro cell line study with patient-derived transcriptome analysis. Patient-derived NSCLC samples and established NSCLC cell lines A549 and NCI-H158 with their cisplatin-resistant variants. Intervention: Bis-(di-4-phenyl-benzylaminethiocarbonyl)disulfide.
A patient subgroup with Z-score >1.5 characterized by ABCC2 and ALDH3A1 overexpression was identified ABCC2 and ALDH3A1 accompany acquisition of cisplatin resistance in A549 cells in vitro Bis-(di-4-phenyl-benzylaminethiocarbonyl)disulfide reverses cisplatin resistance in cisplatin-resistant A549 cells via ALDH and ABCC2 inhibition
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Molecular categorization for ABCC2 and ALDH3A1 overexpression may identify NSCLC patients who could benefit from this novel cisplatin sensitizer. Cell-line heterogeneity in response indicates biomarker-directed therapy will be essential for clinical translation.
In vitro study demonstrates reversal of cisplatin resistance in one cell line via ALDH and ABCC2 inhibition, requiring validation in additional models and clinical testing.
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Molecular categorization for ABCC2 and ALDH3A1 overexpression may identify NSCLC patients who could benefit from this novel cisplatin sensitizer. Cell-line heterogeneity in response indicates biomarker-directed therapy will be essential for clinical translation.
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Background. Lung cancer presents complex etiopathology involving a mix of genetic predispositions and environmental factors. The best treatment modality is surgical resection. However, it becomes ineffective in the advanced metastatic stage. Thus, cisplatin-based chemotherapy, though restricted by an intrinsic and/or acquired chemo-resistant phenotype, remains the first-line therapy for advanced non-small-cell cancer (NSCLC).Methods. Various tools were used to verify the mRNA expression and protein levels of ABC and ALDH proteins in patient-derived non-small-cell lung cancer (NSCLC) samples (GSE102287, GSE43580) and cell lines A549 and NCI-H158 (including their respective cisplatin-resistant variants) to verify the cisplatin-sensitizing abilities of newly synthesized bis-(di-4-phenyl-benzylaminethiocarbonyl)disulfide-non-toxic ALDH and ABCC2 inhibitors.Results. We identified significant molecular differences in the expression levels of ABCC1, ABCC5, ABCC3, ALDH7A1, and ALDH3A1. Additionally, a fairly significant patient subgroup (Z-score > 1.5), characterized by ABCC2 and ALDH3A1 overexpression, was identified. Importantly, in vitro, ABCC2 and ALDH3A1 accompany the acquisition of cisplatin resistance in A549 cells. Bis-(di-4-phenyl-benzylaminethiocarbonyl)disulfide reverses cisplatin resistance in a cisplatin-resistant variant of A549 cells (via ALDH and ABCC2 inhibition) but not in NCI-H158 cells.Conclusions. Molecular categorization of NSCLC cancer is essential for predicting therapy outcomes, enabling the use of bis-(di-4-phenyl-benzylaminethiocarbonyl)disulfide as a cisplatin therapy enhancer for NSCLC patients' subpopulation with significant ABCC2 and ALDH3A1 overexpression.
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