Part of: Cancer Cell Line Encyclopedia (CCLE) project.
Part of: ENCODE project common cell types; tier 3.
Part of: ICBP43 breast cancer cell line panel.
Part of: JFCR39 cancer cell line panel.
Part of: JFCR45 cancer cell line panel.
Part of: KuDOS 95 cell line panel.
Part of: MD Anderson Cell Lines Project.
Part of: NCI60 cancer cell line panel.
Registration: Chiron Master Culture Collection; CMCC 10583 (CMCC #10583).
Doubling time: 1.3 days (PubMed=9671407); 41.9 hours (DTP); 38 hours (ATCC); ~25-30 hours (DSMZ).
Microsatellite instability: Stable (MSS) (PubMed=12661003; Sanger).
Omics: Array-based CGH.
Omics: Cell surface proteome.
Omics: CNV analysis.
Omics: Deep exome analysis.
Omics: Deep proteome analysis.
Omics: Deep RNAseq analysis.
Omics: DNA methylation analysis.
Omics: Metabolome analysis.
Omics: miRNA expression profiling.
Omics: Protein expression by reverse-phase protein arrays.
Omics: Secretome proteome analysis.
Omics: SNP array analysis.
Omics: Transcriptome analysis.
Misspelling: 'MDA-MD-231' in Cosmic 1071900 and Cosmic 1176602.
Misspelling: 'MDA-321' in GEO GSM459713.
Misspelling: 'MDA-MG-231' in PubMed=6582512.
Discontinued: ATCC; CRL-12532.
Derived from metastatic site: Pleural effusion.
TP53 is conventionally thought to prevent cancer formation and progression to metastasis, while mutant TP53 has transforming activities. However, in the clinic, TP53 mutation status does not accurately predict cancer progression. Here we report, based on clinical analysis corroborated with experimental data, that the p53 isoform Δ133p53β promotes cancer cell invasion, regardless of TP53 mutation status. Δ133p53β increases risk of cancer recurrence and death in breast cancer patients. Furthermore Δ133p53β is critical to define invasiveness in a panel of breast and colon cell lines, expressing WT or mutant TP53. Endogenous mutant Δ133p53β depletion prevents invasiveness without affecting mutant full-length p53 protein expression. Mechanistically WT and mutant Δ133p53β induces EMT. Our findings provide explanations to 2 long-lasting and important clinical conundrums: how WT TP53 can promote cancer cell invasion and reciprocally why mutant TP53 gene does not systematically induce cancer progression.
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