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MDA-MB-231

RRID:CVCL_0062

Organism

Homo sapiens

Comments

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 (NCI-DTP); 38 hours (ATCC); ~25-30 hours (DSMZ). Microsatellite instability: Stable (MSS) (PubMed=12661003; Sanger). Sequence variation: TP53 p.Arg280Lys (PubMed=18277095). 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: Fluorescence phenotype profiling. Omics: lncRNA expression profiling. Omics: Metabolome analysis. Omics: miRNA expression profiling. Omics: N-glycan 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.

Proper Citation

NCI-DTP Cat# MDA-MB-231, RRID:CVCL_0062

Category

Cancer cell line

Sex

Female

Synonyms

MDA-MB 231, MDA.MB.231, MDA MB 231, MDA MB231, MDA Mb231, MDA-MB231, MDAMB-231, MDAMB231, MDA-231, MDA231, MB231

Vendor

NCI-DTP

Cat Num

MDA-MB-231

Cross References

BTO; BTO:0000815 CLO; CLO_0007634 EFO; EFO_0001209 MCCL; MCC:0000313 CLDB; cl3402 CLDB; cl3404 CLDB; cl3405 CLDB; cl4945 ATCC; CRL-12532 ATCC; HTB-26 ATCC; CRM-HTB-26 BCRC; 60425 BCRJ; 0164 BioSample; SAMN03472205 CCLE; MDAMB231_BREAST CCRID; 3111C0001CCC000014 CCRID; 3131C0001000700104 ChEMBL-Cells; CHEMBL3307960 ChEMBL-Targets; CHEMBL400 CLS; 300275/p536_MDA-MB-231 Cosmic; 687494 Cosmic; 871146 Cosmic; 875878 Cosmic; 877450 Cosmic; 894087 Cosmic; 897423 Cosmic; 904377 Cosmic; 905960 Cosmic; 934536 Cosmic; 944294 Cosmic; 974235 Cosmic; 991324 Cosmic; 997929 Cosmic; 1010924 Cosmic; 1018477 Cosmic; 1027053 Cosmic; 1044226 Cosmic; 1046950 Cosmic; 1047693 Cosmic; 1071900 Cosmic; 1092613 Cosmic; 1136369 Cosmic; 1152528 Cosmic; 1175833 Cosmic; 1176602 Cosmic; 1176636 Cosmic; 1183773 Cosmic; 1219444 Cosmic; 1287926 Cosmic; 1289395 Cosmic; 1305383 Cosmic; 1309003 Cosmic; 1312370 Cosmic; 1434952 Cosmic; 1436032 Cosmic; 1466805 Cosmic; 1477428 Cosmic; 1481426 Cosmic; 1524347 Cosmic; 1571793 Cosmic; 1609458 Cosmic; 1927242 Cosmic; 1945862 Cosmic; 1998455 Cosmic; 2009512 Cosmic; 2036667 Cosmic; 2164997 Cosmic; 2301528 Cosmic; 2318377 Cosmic; 2361355 Cosmic-CLP; 905960 DSMZ; ACC-732 ECACC; 92020424 GDSC; 905960 GEO; GSM812 GEO; GSM50184 GEO; GSM50248 GEO; GSM69194 GEO; GSM155213 GEO; GSM185093 GEO; GSM185094 GEO; GSM274653 GEO; GSM344349 GEO; GSM344399 GEO; GSM350547 GEO; GSM378148 GEO; GSM388213 GEO; GSM459713 GEO; GSM481304 GEO; GSM587393 GEO; GSM587394 GEO; GSM750781 GEO; GSM799321 GEO; GSM799384 GEO; GSM847036 GEO; GSM847401 GEO; GSM844594 GEO; GSM844595 GEO; GSM887295 GEO; GSM888370 GEO; GSM967818 GEO; GSM1008905 GEO; GSM1053716 GEO; GSM1153390 GEO; GSM1172979 GEO; GSM1172889 GEO; GSM1181242 GEO; GSM1181365 GEO; GSM1214569 GEO; GSM1374651 GEO; GSM1374652 GEO; GSM1401658 GEO; GSM1613823 GEO; GSM1670080 GEO; GSM1833624 GEO; GSM2095710 GEO; GSM2095711 GEO; GSM2124643 ICLC; HTL99004 IZSLER; BS TCL 223 KCB; KCB 200776YJ KCLB; 30026 LINCS_HMS; 50058 LINCS_LDP; LCL-1461 Lonza; 815 NCBI_Iran; C578 NCI-DTP; MDA-MB-231 PRIDE; PXD000239 PRIDE; PXD000397 PRIDE; PXD000691 PRIDE; PXD000914 PRIDE; PXD001553 PRIDE; PXD002192 PRIDE; PXD002649 SKY/M-FISH/CGH; 2815 TOKU-E; 2394 Wikidata; Q17577870

Publications that use this research resource

TP53 drives invasion through expression of its Δ133p53β variant.

  • Gadea G
  • Elife
  • 2016 Sep 15

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.