AKR1C3 as a therapeutic target to overcome erlotinib resistance in lung adenocarcinoma.

Cho WC, Li KP, Wong CF, Fung KY, Chow JCH, Cheung KM, Chan JCH, Lau EYT
Military Medical Research · 2025 · doi:10.1186/s40779-025-00593-4 · PMID:39962616 · PMC11834314
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Additional file 1. Materials and methods. Table S1 Demographic data of lung adenocarcinoma patients. Fig. S1 Examination of the role of AKR1C3 in regulating tumor-initiating cell (T-IC) phenotypes and the correlation of AKR1C3 and resistance development time. Fig. S2 In vitro effect of erlotinib (ER) and AKR1C3 inhibitor 3-{[4-(trifluoromethyl)phenyl]amino}benzoic acid (BA) co-treatment on apoptosis. Fig. S3 Therapeutic potential of erlotinib (ER) combined with AKR1C3 inhibitor 3-{[4- (trifluoromethyl)phenyl]amino}benzoic acid (BA) in ER-resistant lung adenocarcinoma cell line-derived xenograft (CDX) models. Additional file 1. Materials and methods. Table S1 Demographic data of lung adenocarcinoma patients. Fig. S1 Examination of the role of AKR1C3 in regulating tumor-initiating cell (T-IC) phenotypes and the correlation of AKR1C3 and resistance development time. Fig. S2 In vitro effect of erlotinib (ER) and AKR1C3 inhibitor 3-{[4-(trifluoromethyl)phenyl]amino}benzoic acid (BA) co-treatment on apoptosis. Fig. S3 Therapeutic potential of erlotinib (ER) combined with AKR1C3 inhibitor 3-{[4- (trifluoromethyl)phenyl]amino}benzoic acid (BA) in ER-resistant lung adenocarcinoma cell line-derived xenograft (CDX) models.

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