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

Cho WC, Kwan P Li, Li KP, Chi F Wong, Wong CF, King Y Fung, Fung KY, James C H Chow, Chow JCH, Ka M Cheung, Cheung KM, Jeffrey C H Chan, Chan JCH, Lau EYT, Eunice Y T Lau
Military Medical Research · 2025 · vol. 12(1) , pp. 8 · doi:10.1186/s40779-025-00593-4 · PMID:39962616 · PMC11834314
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This research identifies AKR1C3 as a therapeutic target to overcome erlotinib resistance in lung adenocarcinoma, with no mention of endometriosis or adenomyosis.

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This study investigates the role of AKR1C3 in mediating resistance to the tyrosine kinase inhibitor erlotinib within lung adenocarcinoma. The researchers demonstrate that AKR1C3 regulates tumor-initiating cell phenotypes and correlates with the time required for resistance development in patient-derived models. In vitro and in vivo experiments reveal that co-treatment with an AKR1C3 inhibitor restores sensitivity to erlotinib in resistant cell lines and xenograft models. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Supplementary Material

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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