0000000000298257

AUTHOR

Sylvie Lantuejoul

showing 3 related works from this author

NLRP3 controls ATM activation in response to DNA damage

2020

The DNA damage response (DDR) is essential to preserve genomic integrity and acts as a barrier to cancer. The ATM pathway orchestrates the cellular response to DNA double strand breaks (DSBs), and its attenuation is frequent during tumorigenesis. Here, we show that NLRP3, a Pattern Recognition Receptor known for its role in the inflammasome complex formation, interacts with the ATM kinase to control the early phase of DDR, independently of its inflammasome activity. NLRP3 down-regulation in human bronchial epithelial cells impairs ATM pathway activation as shown by an altered ATM substrate phosphorylation profile, and due to impaired p53 activation, confers resistance to acute genomic stres…

DNA damage[SDV]Life Sciences [q-bio]medicine.disease_cause03 medical and health sciencesSubstrate-level phosphorylationchemistry.chemical_compound0302 clinical medicineDNA Damage Signalingmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyCancer0303 health sciencesInnate immune systemintegumentary systemChemistryNLRP3 receptorPattern recognition receptorInflammasome3. Good healthCell biology[SDV] Life Sciences [q-bio]030220 oncology & carcinogenesisCarcinogenesisInflammasome complexDNAmedicine.drug
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Abstract 3940: Inactivation of the PARD3 gene is a recurrent event in lung squamous cell carcinomas and affects STAT3 activity and tumor invasiveness

2015

Abstract Correct apicobasal polarization and intercellular adhesions are essential for the appropriate development of normal epithelia. Here, we investigated the contribution of the partitioning defective 3 gene, PARD3, to the carcinogenesis of lung squamous cell carcinomas (LSCCs). Tumor-specific PARD3 alterations were found in eight per cent of the tumors, placing PARD3 among the most common tumor suppressor genes in LSCC. Some PAR3 mutant proteins prevented the formation of contacts between neighboring cells, i.e. had reduced ability to form tight junctions and actin-based protrusions. This affected subsequent downstream signaling, i.e. binding to aPKC and activation of RAC1. Further, we…

Cancer ResearchConfluencyPARD3 GeneCellWild typeRAC1Biologymedicine.diseasemedicine.disease_causeMetastasismedicine.anatomical_structureOncologymedicineCancer researchCell adhesionCarcinogenesisCancer Research
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PARD3 Inactivation in Lung Squamous Cell Carcinomas Impairs STAT3 and Promotes Malignant Invasion.

2015

Abstract Correct apicobasal polarization and intercellular adhesions are essential for the appropriate development of normal epithelia. Here, we investigated the contribution of the cell polarity regulator PARD3 to the development of lung squamous cell carcinomas (LSCC). Tumor-specific PARD3 alterations were found in 8% of LSCCs examined, placing PARD3 among the most common tumor suppressor genes in this malignancy. Most PAR3-mutant proteins exhibited a relative reduction in the ability to mediate formation of tight junctions and actin-based protrusions, bind atypical protein kinase C, activate RAC1, and activate STAT3 at cell confluence. Thus, PARD3 alterations prevented the formation of c…

STAT3 Transcription Factorrac1 GTP-Binding ProteinCancer ResearchLung NeoplasmsCellMice NudeRAC1Cell Cycle ProteinsBiologyArticleCell MovementCell Line TumorCell polaritymedicineAnimalsHumansNeoplasm InvasivenessProtein Kinase CAdaptor Proteins Signal TransducingCell ProliferationConfluencyTight junctionBase SequenceCell growthLiver NeoplasmsMembrane ProteinsSequence Analysis DNACell biologymedicine.anatomical_structureOncologyCell cultureMutationCancer researchCarcinoma Squamous CellTranscriptomeIntracellularNeoplasm TransplantationCancer research
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