Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA326127 | ENA |
REPOSITORIES: ENA
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Project description:Microarray expression data generated to determine the impact of defined p53 mutations on lung cancer cell phenotypes, and on the tumour supressive responses induced by WT p53 restoration. In murine models of lung cancer, the therapeutic benefit of WT p53 restoration has been demonstrated in p53-deficient tumours (Juntilla et al, 2010; Feldser et al, 2010). However, it remains unknown if the restoration of WT p53 function is beneficial in p53 mutant tumours. Thus, to determine the impact of p53-targeted therapy in mutant p53 lung cancer, we analysed cells from murine lung tumours of distinct p53 genotypes. Utilising the well characterised p53-ER allele (Christophorou et al, 2005; Martins et al, 2006; Juntilla et al, 2010) we carried out transcriptional profiling of KrasG12D/+ cell lines isolated from advanced lung tumours with defined p53 status: p53Fx/ER (null), p53R270H/ER and p53R172H/ER in the absence (p53 WT OFF) or presence (p53 WT ON) of 4-hydroxytamoxifen (4-OHT). The temporal specificity of p53-ER restoration allowed us to utilised two timepoints to determine both the immediate (2hr) and sustained (8hr) impact of WT p53 function.
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Project description:This SuperSeries is composed of the following subset Series: GSE23873: Stage-specific sensitivity to p53 restoration in lung cancer: cell line data GSE23874: Stage-specific sensitivity to p53 restoration in lung cancer: tumor data Refer to individual Series
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Project description:Inactivation of the retinoblastoma (RB) tumor suppressor in lung adenocarcinoma is associated with the rapid acquisition of metastatic ability and the loss of lung cell lineage commitment. We previously showed that restoration of RB in advanced lung adenocarcinomas in the mouse was correlated with a decreased frequency of lineage de-committed tumors and overt metastases. To identify a causal relationship for RB and its role in reprogramming lineage commitment and reducing metastatic competency in lung adenocarcinoma, we developed multiple tumor spheroid forming lines where RB restoration could be achieved after characterization of the degree of each spheroid’s lineage commitment and metastatic ability. Surprisingly, we discovered that RB inactivation dramatically promoted tumor spheroid forming potential in tumors that arise in the KrasLSL-G12D/+; p53flox/flox lung adenocarcinoma model. However, RB reactivation had no effect on the maintenance of tumor spheroid lines once established. Additionally, we show that RB-deficient tumor spheroid lines are not uniformly metastatically competent but are equally likely to be non-metastatic. Interestingly, unlike tumor spheroid maintenance, RB restoration could functionally revert metastatic tumor spheroids to a non-metastatic cell state. Thus, strategies to reinstate RB-pathway activity in lung cancer may reverse metastatic ability and have therapeutic potential. Finally, the acquisition of tumor spheroid forming potential reflects underlying cell state plasticity, which is often predictive of, or even conflated with metastatic ability. Our data support that each is a discrete cell state restricted by RB and question the suitability of tumor spheroid models for their predictive potential of advanced metastatic tumor cell states.
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