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Homo sapiens


Part of: AKT genetic alteration cell panel (ATCC TCP-1029). Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: EGFR genetic alteration cell panel (ATCC TCP-1027). Part of: ERK genetic alteration cell panel (ATCC TCP-1033). Part of: ICBP43 breast cancer cell line panel. Part of: KuDOS 95 cell line panel. Part of: MD Anderson Cell Lines Project. Part of: Naval Biosciences Laboratory (NBL) collection (transferred to ATCC in 1982). Doubling time: 3.5 days (PubMed=9671407); 78 hours (PubMed=25984343); ~100 hours (DSMZ). Microsatellite instability: Stable (MSS) (PubMed=23671654; Sanger). Sequence variation: Heterozygous for MAPK1 p.His61Gln (ATCC). Omics: Array-based CGH. Omics: CNV analysis. Omics: Deep exome analysis. Omics: Deep phosphoproteome analysis. Omics: Deep proteome analysis. Omics: Deep RNAseq analysis. Omics: DNA methylation analysis. Omics: Genome sequenced. Omics: Metabolome analysis. Omics: miRNA expression profiling. Omics: Protein expression by reverse-phase protein arrays. Omics: shRNA library screening. Omics: SNP array analysis. Omics: Transcriptome analysis. Discontinued: ATCC; CRL-7913.

Proper Citation

ATCC Cat# CRL-7913, RRID:CVCL_0179


Cancer cell line




BT474, Bt-474



Cat Num


Cross References

BTO; BTO:0001932 CLO; CLO_0002042 EFO; EFO_0001093 MCCL; MCC:0000070 CLDB; cl497 CLDB; cl498 CLDB; cl4997 AddexBio; C0006012/4902 ATCC; CRL-7913 ATCC; HTB-20 BCRC; 60359 BCRJ; 0353 BioSample; SAMN01821539 BioSample; SAMN01821618 BioSample; SAMN03473029 BioSamples; SAMEA3516847 BioSamples; SAMEA3516848 BioSamples; SAMEA3516849 CCLE; BT474_BREAST CCRID; 3111C0001CCC000129 CCRID; 3111C0002000000023 CCRID; 3131C0001000700143 ChEMBL-Cells; CHEMBL3307636 ChEMBL-Targets; CHEMBL614529 CLS; 300131/p705_BT-474 Cosmic; 687464 Cosmic; 871138 Cosmic; 904351 Cosmic; 923058 Cosmic; 934520 Cosmic; 946359 Cosmic; 970088 Cosmic; 979721 Cosmic; 1000122 Cosmic; 1017168 Cosmic; 1018460 Cosmic; 1046934 Cosmic; 1047699 Cosmic; 1071903 Cosmic; 1129654 Cosmic; 1136353 Cosmic; 1176605 Cosmic; 1287890 Cosmic; 1289383 Cosmic; 1308996 Cosmic; 1434947 Cosmic; 1523771 Cosmic; 1603191 Cosmic; 1609475 Cosmic; 1945863 Cosmic; 2165003 Cosmic; 2301523 Cosmic; 2318376 Cosmic; 2361356 Cosmic-CLP; 946359 DSMZ; ACC-64 GDSC; 946359 GEO; GSM1716 GEO; GSM1725 GEO; GSM69198 GEO; GSM73557 GEO; GSM73702 GEO; GSM115110 GEO; GSM147888 GEO; GSM147957 GEO; GSM149981 GEO; GSM149989 GEO; GSM149997 GEO; GSM155210 GEO; GSM184392 GEO; GSM184393 GEO; GSM213707 GEO; GSM213717 GEO; GSM213718 GEO; GSM213719 GEO; GSM213737 GEO; GSM213740 GEO; GSM213743 GEO; GSM213745 GEO; GSM217615 GEO; GSM274657 GEO; GSM276780 GEO; GSM320173 GEO; GSM344341 GEO; GSM344391 GEO; GSM350504 GEO; GSM388211 GEO; GSM533397 GEO; GSM533412 GEO; GSM590105 GEO; GSM679677 GEO; GSM679678 GEO; GSM679679 GEO; GSM679680 GEO; GSM679681 GEO; GSM679682 GEO; GSM679683 GEO; GSM679684 GEO; GSM679685 GEO; GSM679686 GEO; GSM679687 GEO; GSM679688 GEO; GSM679689 GEO; GSM679690 GEO; GSM679691 GEO; GSM783958 GEO; GSM847198 GEO; GSM847453 GEO; GSM843476 GEO; GSM886892 GEO; GSM887957 GEO; GSM903063 GEO; GSM903064 GEO; GSM903065 GEO; GSM903066 GEO; GSM903067 GEO; GSM903068 GEO; GSM903069 GEO; GSM967821 GEO; GSM1008891 GEO; GSM1053692 GEO; GSM1172941 GEO; GSM1172853 GEO; GSM1214587 GEO; GSM1264068 GEO; GSM1264073 GEO; GSM1264110 GEO; GSM1264115 GEO; GSM1374408 GEO; GSM1374409 GEO; GSM1374410 GEO; GSM1401649 GEO; GSM1669630 GEO; GSM2176271 GEO; GSM2176272 ICLC; HTL00008 IGRhCellID; BT474 KCB; KCB 2011115YJ KCLB; 60062 LINCS_HMS; 50106 LINCS_LDP; LCL-1308 NCBI_Iran; C435 PRIDE; PXD002281 PRIDE; PXD004357 TOKU-E; 694

Publications that use this research resource

Environmental cystine drives glutamine anaplerosis and sensitizes cancer cells to glutaminase inhibition.

  • Muir A
  • Elife
  • 2017 Aug 15

Literature context: D:CVCL_0179; MCF7: ATCC Cat# HTB-22, RRID:C


Many mammalian cancer cell lines depend on glutamine as a major tri-carboxylic acid (TCA) cycle anaplerotic substrate to support proliferation. However, some cell lines that depend on glutamine anaplerosis in culture rely less on glutamine catabolism to proliferate in vivo. We sought to understand the environmental differences that cause differential dependence on glutamine for anaplerosis. We find that cells cultured in adult bovine serum, which better reflects nutrients available to cells in vivo, exhibit decreased glutamine catabolism and reduced reliance on glutamine anaplerosis compared to cells cultured in standard tissue culture conditions. We find that levels of a single nutrient, cystine, accounts for the differential dependence on glutamine in these different environmental contexts. Further, we show that cystine levels dictate glutamine dependence via the cystine/glutamate antiporter xCT/SLC7A11. Thus, xCT/SLC7A11 expression, in conjunction with environmental cystine, is necessary and sufficient to increase glutamine catabolism, defining important determinants of glutamine anaplerosis and glutaminase dependence in cancer.

TGF-β reduces DNA ds-break repair mechanisms to heighten genetic diversity and adaptability of CD44+/CD24- cancer cells.

  • Pal D
  • Elife
  • 2017 Jan 16

Literature context: , BT-474 (RRID:CVCL_0179), MDA-MB-2


Many lines of evidence have indicated that both genetic and non-genetic determinants can contribute to intra-tumor heterogeneity and influence cancer outcomes. Among the best described sub-population of cancer cells generated by non-genetic mechanisms are cells characterized by a CD44+/CD24- cell surface marker profile. Here, we report that human CD44+/CD24- cancer cells are genetically highly unstable because of intrinsic defects in their DNA-repair capabilities. In fact, in CD44+/CD24- cells, constitutive activation of the TGF-beta axis was both necessary and sufficient to reduce the expression of genes that are crucial in coordinating DNA damage repair mechanisms. Consequently, we observed that cancer cells that reside in a CD44+/CD24- state are characterized by increased accumulation of DNA copy number alterations, greater genetic diversity and improved adaptability to drug treatment. Together, these data suggest that the transition into a CD44+/CD24- cell state can promote intra-tumor genetic heterogeneity, spur tumor evolution and increase tumor fitness.

Funding information:
  • NCI NIH HHS - P01 CA129243()
  • NCI NIH HHS - P30 CA045508()