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T25
Cell line name BT-549
Synonyms BT 549; BT.549; BT549
Accession CVCL_1092
Resource Identification Initiative To cite this cell line use: BT-549 (RRID:CVCL_1092)
Comments Group: Triple negative breast cancer (TNBC) cell line.
Part of: Cancer Dependency Map project (DepMap) (includes Cancer Cell Line Encyclopedia - CCLE).
Part of: COSMIC cell lines project.
Part of: JWGray breast cancer cell line panel.
Part of: ICBP43 breast cancer cell line panel.
Part of: KuDOS 95 cell line panel.
Part of: MD Anderson Cell Lines Project.
Part of: NCI-60 cancer cell line panel.
Population: Caucasian.
Doubling time: 3.7 days (PubMed=9671407); 51 hours (PubMed=25984343); 53.9 hours (NCI-DTP=BT-549); 25.46 hours (JWGray panel).
Microsatellite instability: Stable (MSS) (Sanger).
Omics: Array-based CGH.
Omics: CNV analysis.
Omics: Deep exome analysis.
Omics: Deep proteome analysis.
Omics: Deep quantitative proteome analysis.
Omics: DNA methylation analysis.
Omics: Fluorescence phenotype profiling.
Omics: Glycoproteome analysis by proteomics.
Omics: lncRNA expression profiling.
Omics: miRNA expression profiling.
Omics: Metabolome analysis.
Omics: Protein expression by reverse-phase protein arrays.
Omics: SNP array analysis.
Omics: Transcriptome analysis by microarray.
Omics: Transcriptome analysis by RNAseq.
Misspelling: HTB-122; Note=Based on the ATCC catalog number.
Derived from site: In situ; Breast; UBERON=UBERON_0000310.
PubMed=21552935; DOI=10.3892/ijo.7.5.1079
Nangia-Makker P., Thompson E., Hogan C., Ochieng J., Raz A.
Induction of tumorigenicity by galectin-3 in a nontumorigenic human breast-carcinoma cell-line.
Int. J. Oncol. 7:1079-1087(1995)
PubMed=9561029
Warfield P.R., Nangia-Makker P., Raz A., Ochieng J.
Adhesion of human breast carcinoma to extracellular matrix proteins is modulated by galectin-3.
Invasion Metastasis 17:101-112(1997)
PubMed=9671407; DOI=10.1038/sj.onc.1201814
Sweeney K.J., Swarbrick A., Sutherland R.L., Musgrove E.A.
Lack of relationship between CDK activity and G1 cyclin expression in breast cancer cells.
Oncogene 16:2865-2878(1998)
PubMed=10700174; DOI=10.1038/73432
Ross D.T., Scherf U., Eisen M.B., Perou C.M., Rees C., Spellman P.T., Iyer V.R., Jeffrey S.S., van de Rijn M., Waltham M.C., Pergamenschikov A., Lee J.C.F., Lashkari D., Shalon D., Myers T.G., Weinstein J.N., Botstein D., Brown P.O.
Systematic variation in gene expression patterns in human cancer cell lines.
Nat. Genet. 24:227-235(2000)
PubMed=10862037; DOI=10.1002/1098-2264(200007)28:3<308::AID-GCC9>3.0.CO;2-B
Kytola S., Rummukainen J., Nordgren A., Karhu R., Farnebo F., Isola J.J., Larsson C.
Chromosomal alterations in 15 breast cancer cell lines by comparative genomic hybridization and spectral karyotyping.
Genes Chromosomes Cancer 28:308-317(2000)
PubMed=10969801
Forozan F., Mahlamaki E.H., Monni O., Chen Y.-D., Veldman R., Jiang Y., Gooden G.C., Ethier S.P., Kallioniemi A.H., Kallioniemi O.-P.
Comparative genomic hybridization analysis of 38 breast cancer cell lines: a basis for interpreting complementary DNA microarray data.
Cancer Res. 60:4519-4525(2000)
PubMed=11343771; DOI=10.1016/S0165-4608(00)00387-3
Rummukainen J., Kytola S., Karhu R., Farnebo F., Larsson C., Isola J.J.
Aberrations of chromosome 8 in 16 breast cancer cell lines by comparative genomic hybridization, fluorescence in situ hybridization, and spectral karyotyping.
Cancer Genet. Cytogenet. 126:1-7(2001)
PubMed=15153330; DOI=10.1593/neo.3292; PMCID=PMC1502105
Watts G.S., Oshiro M.M., Junk D.J., Wozniak R.J., Watterson S.J., Domann F.E., Futscher B.W.
The acetyltransferase p300/CBP-associated factor is a p53 target gene in breast tumor cells.
Neoplasia 6:187-194(2004)
PubMed=15677628; DOI=10.1093/carcin/bgi032
Gorringe K.L., Chin S.-F., Pharoah P.D.P., Staines J.M., Oliveira C., Edwards P.A.W., Caldas C.
Evidence that both genetic instability and selection contribute to the accumulation of chromosome alterations in cancer.
Carcinogenesis 26:923-930(2005)
PubMed=15748285; DOI=10.1186/1479-5876-3-11; PMCID=PMC555742
Adams S., Robbins F.-M., Chen D., Wagage D., Holbeck S.L., Morse H.C. 3rd, Stroncek D., Marincola F.M.
HLA class I and II genotype of the NCI-60 cell lines.
J. Transl. Med. 3:11.1-11.8(2005)
PubMed=16397213; DOI=10.1158/0008-5472.CAN-05-2853
Elstrodt F., Hollestelle A., Nagel J.H.A., Gorin M., Wasielewski M., van den Ouweland A.M.W., Merajver S.D., Ethier S.P., Schutte M.
BRCA1 mutation analysis of 41 human breast cancer cell lines reveals three new deleterious mutants.
Cancer Res. 66:41-45(2006)
PubMed=16541312; DOI=10.1007/s10549-006-9186-z
Wasielewski M., Elstrodt F., Klijn J.G.M., Berns E.M.J.J., Schutte M.
Thirteen new p53 gene mutants identified among 41 human breast cancer cell lines.
Breast Cancer Res. Treat. 99:97-101(2006)
PubMed=17088437; DOI=10.1158/1535-7163.MCT-06-0433; PMCID=PMC2705832
Ikediobi O.N., Davies H.R., Bignell G.R., Edkins S., Stevens C., O'Meara S., Santarius T., Avis T., Barthorpe S., Brackenbury L., Buck G., Butler A.P., Clements J., Cole J., Dicks E., Forbes S., Gray K., Halliday K., Harrison R., Hills K., Hinton J., Hunter C., Jenkinson A., Jones D., Kosmidou V., Lugg R., Menzies A., MirT., Parker A., Perry J., Raine K.M., Richardson D., Shepherd R., Small A., Smith R., Solomon H., Stephens P.J., Teague J.W., Tofts C., Varian J., Webb T., West S., Widaa S., Yates A., Reinhold W.C., Weinstein J.N., Stratton M.R., Futreal P.A., Wooster R.
Mutation analysis of 24 known cancer genes in the NCI-60 cell line set.
Mol. Cancer Ther. 5:2606-2612(2006)
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文献和实验*发表【中文论文】请标注:由博辉生物科技(广州)有限公司提供; *发表【英文论文】请标注:From Bohui Biological Technology (Guangzhou) Co., Ltd.
「癌细胞」:是我杀了我?PNAS 这项研究竟让肿瘤自己杀死自己
)具有相似的分子特性。 图片来源:PNAS BT474 作为 HER2 阳性肿瘤模型 为了确定用于旁分泌研究的最佳肿瘤模型,研究人员评估了两种 HER2 阳性肿瘤细胞系(SKOV3ip 和 BT474)的 HER2 水平,转导效率,抗体表达水平和 TZB 敏感性。结果发现相对于对照细胞系,HER2 水平在 BT474 细胞系中最高。天然腺病毒受体水平在对照 HEK293 细胞中最高,在 A549 和 BT474 细胞中分别降低 57% 和 67%,而在 SKOV3ip 中最低。体外转导效率方面,BT
Cancer Cell:整合素 αvβ6-TGFβ-SOX4 途径驱动三阴性乳腺癌的免疫逃逸
1、TAP2、PSMB9、HLA-B 和 HLA-c)。这些数据表明 SOX4 在调节肿瘤细胞先天性免疫和适应性免疫途径中起作用。图片来源:Cancer Cell抑制 SOX4 通路是否能提高 MHC-I low 肿瘤细胞对 CD8+T 细胞的敏感性?MHC-I 的突变和失活通常是肿瘤细胞免疫逃逸的基础。为研究 SOX4 在 MHC-I 的突变和失活肿瘤细胞的作用,研究者将 BT549 细胞进行分选 HLA low 和 HLA high BT549 肿瘤细胞。HLA low 肿瘤细胞的 SOX4
superskyfly 我自己都觉得我自己很牛,千百人都做出来的试验,我就是做不出来。质粒用的是Promega p4.32-NF-kB-Luc, 转染用的是Invitrogen的Lipofactamin, 激活用的是Sigma生产的PMA和PHA-P,Assay用的是Promega dual,结果加了PMA和PHA的和不加的读数几乎没有区别。加了compound的和不加的也没有区别。 用过PC3, Jurkat, A549,HCT116都是一样。
技术资料





