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 modelPROTAC EZH2 degrader-1 overcomes the resistance of podophyllotoxin derivatives in refractory small cell lung cancer with leptomeningeal metastasis
Shi M, Ding X, Tang L, Cao W, Su B, Zhang J. PROTAC EZH2 degrader-1 overcomes the resistance of podophyllotoxin derivatives in refractory small cell lung cancer with leptomeningeal metastasis. BMC Cancer 2024, 24: 504. PMID: 38644473, PMCID: PMC11034131, DOI: 10.1186/s12885-024-12244-3.Peer-Reviewed Original ResearchConceptsSmall cell lung cancerCell lung cancerMouse modelLung cancerRefractory small cell lung cancerNude miceIn vivo drug testingCell linesDrug testingLM cellsSensitivity of cisplatinIn vitro drug testingIncreased in vitroBackgroundLeptomeningeal metastasisLeptomeningeal metastasesSevere neurological disordersAssociated with several neurological disordersDrug sensitivityIn vivo live imagingHistological examinationCarotid arteryEffective treatmentMetastasisDrug trialsExpressing luciferaseTransformation 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