Disulfiram/copper complex improves the effectiveness of the WEE1 inhibitor Adavosertib in p53 deficient non-small cell lung cancer via ferroptosis
Liu D, Cao J, Ding X, Xu W, Yao X, Dai M, Tai Q, Shi M, Fei K, Xu Y, Su B. Disulfiram/copper complex improves the effectiveness of the WEE1 inhibitor Adavosertib in p53 deficient non-small cell lung cancer via ferroptosis. Biochimica Et Biophysica Acta (BBA) - Molecular Basis Of Disease 2024, 1870: 167455. PMID: 39111630, DOI: 10.1016/j.bbadis.2024.167455.Peer-Reviewed Original ResearchWEE1 inhibitorNon-small cell lung cancerNSCLC cellsCell lung cancerSynergistic therapeutic approachesProtein levelsEffective treatment strategiesPro-oxidant drugsKinase activity of Wee1P53-deficient cellsActivity of Wee1Tumor volumeCombination therapyDSF-CuRepurposing disulfiramTumor weightSolute carrier family 7 memberWee1 protein levelsP53 deficiencyPoor prognosisReduced cell viabilityFunctional p53Lung cancerTreatment strategiesXenograft modelTransformation to small cell lung cancer is irrespective of EGFR and accelerated by SMAD4-mediated ASCL1 transcription independently of RB1 in non-small cell lung cancer
Ding X, Shi M, Liu D, Cao J, Zhang K, Zhang R, Zhang L, Ai K, Su B, Zhang J. Transformation to small cell lung cancer is irrespective of EGFR and accelerated by SMAD4-mediated ASCL1 transcription independently of RB1 in non-small cell lung cancer. Cell Communication And Signaling 2024, 22: 45. PMID: 38233864, PMCID: PMC10795321, DOI: 10.1186/s12964-023-01260-8.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerSmall cell lung cancerSmall cell lung cancer transformationCell lung cancerTransformation to small cell lung cancerLung cancerEGFR-mutant non-small cell lung cancerMYC inhibitorsNon-small cell lung cancer patientsMechanisms of TKI resistanceEGFR mutation statusResistant lung cancerNon-small cell lung cancer cellsDriver gene statusPhenotype in vitroCancer-related genesPotential functional genesPutative gene functionsCRISPR-Cas 9SCLC transformationTKI resistanceMutation statusNeuroendocrine phenotypeRB1 statusClinical characteristics