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Homo sapiens


Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: ENCODE project common cell types; tier 2. Part of: JFCR39 cancer cell line panel. Part of: JFCR45 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: NCI60 cancer cell line panel. Registration: Chiron Master Culture Collection; CMCC 10377 (CMCC #10377). Doubling time: 1.8 days (PubMed=9671407); 80 hours (PubMed=25984343); 31.2 hours (PubMed=22628656); 25.4 hours (NCI-DTP); ~50 hours, with a range of 30-72 hours (DSMZ). Microsatellite instability: Stable (MSS) (PubMed=12661003; PubMed=23671654; Sanger). Omics: Array-based CGH. Omics: CNV analysis. Omics: Deep antibody staining analysis. Omics: Deep exome analysis. Omics: Deep phosphoproteome analysis. Omics: Deep proteome analysis. Omics: Deep RNAseq analysis. Omics: DNA methylation analysis. Omics: Fluorescence phenotype profiling. Omics: H3K4me3 ChIP-seq epigenome analysis. Omics: lncRNA expression profiling. Omics: Metabolome analysis. Omics: miRNA expression profiling. Omics: N-glycan profiling. Omics: Protein expression by reverse-phase protein arrays. Omics: shRNA library screening. Omics: SNP array analysis. Omics: Transcriptome analysis. Omics: Virome analysis using proteomics. Anecdotal: This is the first hormone-responsive breast cancer cell line to have been established. Anecdotal: Helen Mallon (sister Catherine Frances), the patient from which this cell line is derived was a nun (Sister Catherine Frances) at the Immaculate Heart of Mary Convent in Monroe, Michigan. Misspelling: 'MFC-7'in ChEMBL CHEMBL614345 and CHEMBL3307491. Discontinued: ATCC; CRL-12584. Discontinued: JCRB; NIHS0200. Derived from metastatic site: Pleural effusion.

Proper Citation



Cancer cell line




MCF 7, MCF.7, MCF7, Michigan Cancer Foundation-7, ssMCF-7, ssMCF7, MCF7/WT, IBMF-7, MCF7-CTRL



Cat Num


Cross References

BTO; BTO:0000093 CLO; CLO_0007601 CLO; CLO_0007605 CLO; CLO_0007606 CLO; CLO_0050868 EFO; EFO_0001203 MCCL; MCC:0000307 CLDB; cl3366 CLDB; cl3367 CLDB; cl3368 CLDB; cl3369 CLDB; cl3370 CLDB; cl3371 CLDB; cl3372 CLDB; cl3373 CLDB; cl3375 ATCC; CRL-12584 ATCC; HTB-22 BCRC; 60436 BCRJ; 0162 BioSample; SAMN01821575 BioSample; SAMN01821646 BioSample; SAMN01821698 BioSample; SAMN03473276 CCLE; MCF7_BREAST CCRID; 3111C0001CCC000013 CCRID; 3111C0001CCC000328 CCRID; 3131C0001000700074 CCRID; 3142C0001000000054 ChEMBL-Cells; CHEMBL3307491 ChEMBL-Cells; CHEMBL3308403 ChEMBL-Targets; CHEMBL387 ChEMBL-Targets; CHEMBL614345 CLS; 300273/p2720_MCF-7 Cosmic; 687490 Cosmic; 755293 Cosmic; 809239 Cosmic; 871143 Cosmic; 875876 Cosmic; 877449 Cosmic; 894096 Cosmic; 897419 Cosmic; 904373 Cosmic; 905946 Cosmic; 912001 Cosmic; 921976 Cosmic; 923059 Cosmic; 934534 Cosmic; 944293 Cosmic; 947352 Cosmic; 949189 Cosmic; 970089 Cosmic; 979723 Cosmic; 991328 Cosmic; 997916 Cosmic; 1000123 Cosmic; 1010932 Cosmic; 1017161 Cosmic; 1018463 Cosmic; 1019310 Cosmic; 1046936 Cosmic; 1047712 Cosmic; 1066224 Cosmic; 1071901 Cosmic; 1092612 Cosmic; 1102382 Cosmic; 1136341 Cosmic; 1152527 Cosmic; 1175832 Cosmic; 1176603 Cosmic; 1176648 Cosmic; 1183770 Cosmic; 1287893 Cosmic; 1289391 Cosmic; 1305382 Cosmic; 1308991 Cosmic; 1312369 Cosmic; 1326278 Cosmic; 1434950 Cosmic; 1436031 Cosmic; 1477426 Cosmic; 1481420 Cosmic; 1523770 Cosmic; 1524349 Cosmic; 1571788 Cosmic; 1603215 Cosmic; 1609459 Cosmic; 1945860 Cosmic; 1995500 Cosmic; 1998454 Cosmic; 2162161 Cosmic; 2165024 Cosmic; 2301233 Cosmic; 2301526 Cosmic; 2307194 Cosmic; 2318370 Cosmic; 2361358 Cosmic; 2525755 Cosmic; 2553502 Cosmic-CLP; 905946 DSMZ; ACC-115 ECACC; 86012803 ENCODE; ENCBS000AAA ENCODE; ENCBS001AAA ENCODE; ENCBS017ENC ENCODE; ENCBS034XKZ ENCODE; ENCBS036ENC ENCODE; ENCBS037ENC ENCODE; ENCBS050QMU ENCODE; ENCBS053YJT ENCODE; ENCBS056AAA ENCODE; ENCBS094ENC ENCODE; ENCBS095ENC ENCODE; ENCBS096ENC ENCODE; ENCBS097ENC ENCODE; ENCBS098ENC ENCODE; ENCBS102ENC ENCODE; ENCBS103ENC ENCODE; ENCBS104ENC ENCODE; ENCBS105ENC ENCODE; ENCBS108ENC ENCODE; ENCBS123ZGI ENCODE; ENCBS134PJO ENCODE; ENCBS135SOE ENCODE; ENCBS143XXF ENCODE; ENCBS155VQC ENCODE; ENCBS158RRU ENCODE; ENCBS168ISE ENCODE; ENCBS174OTK ENCODE; ENCBS200IWR ENCODE; ENCBS216AOQ ENCODE; ENCBS236AAA ENCODE; ENCBS237AAA ENCODE; ENCBS240AAA ENCODE; ENCBS241AAA ENCODE; ENCBS242AAA ENCODE; ENCBS243AAA ENCODE; ENCBS244AAA ENCODE; ENCBS245AAA ENCODE; ENCBS246AAA ENCODE; ENCBS247AAA ENCODE; ENCBS248AAA ENCODE; ENCBS249AAA ENCODE; ENCBS250AAA ENCODE; ENCBS251AAA ENCODE; ENCBS252AAA ENCODE; ENCBS254AYH ENCODE; ENCBS267CRP ENCODE; ENCBS308QKF ENCODE; ENCBS325VCY ENCODE; ENCBS328UKJ ENCODE; ENCBS331EJR ENCODE; ENCBS488MMM ENCODE; ENCBS496HCC ENCODE; ENCBS530DHL ENCODE; ENCBS536NWC ENCODE; ENCBS546VBU ENCODE; ENCBS547AXB ENCODE; ENCBS564FRY ENCODE; ENCBS567IJO ENCODE; ENCBS581MUA ENCODE; ENCBS584TFV ENCODE; ENCBS609QTY ENCODE; ENCBS614ENC ENCODE; ENCBS615ENC ENCODE; ENCBS616ENC ENCODE; ENCBS616MBU ENCODE; ENCBS661RDG ENCODE; ENCBS670IYV ENCODE; ENCBS705BBA ENCODE; ENCBS747ZRJ ENCODE; ENCBS748WRO ENCODE; ENCBS789UPK ENCODE; ENCBS866ZXX ENCODE; ENCBS867ORK ENCODE; ENCBS873NNF ENCODE; ENCBS912WOF ENCODE; ENCBS957OEW ENCODE; ENCBS959SHH ENCODE; ENCBS967MVZ ENCODE; ENCBS974BZV GDSC; 905946 GEO; GSM1723 GEO; GSM50183 GEO; GSM50247 GEO; GSM69199 GEO; GSM73693 GEO; GSM115111 GEO; GSM155207 GEO; GSM156025 GEO; GSM185091 GEO; GSM185092 GEO; GSM211175 GEO; GSM274640 GEO; GSM276773 GEO; GSM276774 GEO; GSM276775 GEO; GSM276776 GEO; GSM276777 GEO; GSM276778 GEO; GSM276779 GEO; GSM320172 GEO; GSM344347 GEO; GSM344397 GEO; GSM350552 GEO; GSM378140 GEO; GSM388212 GEO; GSM459726 GEO; GSM472936 GEO; GSM481303 GEO; GSM510510 GEO; GSM533396 GEO; GSM533413 GEO; GSM590108 GEO; GSM679692 GEO; GSM679693 GEO; GSM679694 GEO; GSM739996 GEO; GSM739997 GEO; GSM739998 GEO; GSM750771 GEO; GSM750777 GEO; GSM750778 GEO; GSM750801 GEO; GSM783949 GEO; GSM799320 GEO; GSM799383 GEO; GSM816627 GEO; GSM816670 GEO; GSM827593 GEO; GSM847394 GEO; GSM847490 GEO; GSM844586 GEO; GSM844587 GEO; GSM887291 GEO; GSM888366 GEO; GSM945269 GEO; GSM945274 GEO; GSM967819 GEO; GSM967823 GEO; GSM1008565 GEO; GSM1008581 GEO; GSM1008603 GEO; GSM1008904 GEO; GSM1029440 GEO; GSM1029441 GEO; GSM1029442 GEO; GSM1029443 GEO; GSM1029444 GEO; GSM1029445 GEO; GSM1029446 GEO; GSM1029447 GEO; GSM1029448 GEO; GSM1029449 GEO; GSM1040306 GEO; GSM1040376 GEO; GSM1053687 GEO; GSM1068138 GEO; GSM1068139 GEO; GSM1153389 GEO; GSM1172885 GEO; GSM1181258 GEO; GSM1181263 GEO; GSM1214589 GEO; GSM1374643 GEO; GSM1374644 GEO; GSM1374645 GEO; GSM1401653 GEO; GSM1670076 GEO; GSM1833626 GEO; GSM2046560 GEO; GSM2046561 GEO; GSM2046562 GEO; GSM2046563 GEO; GSM2046564 GEO; GSM2046565 GEO; GSM2046566 GEO; GSM2046567 GEO; GSM2046568 GEO; GSM2046569 GEO; GSM2046570 GEO; GSM2046571 GEO; GSM2046572 GEO; GSM2046573 GEO; GSM2046574 GEO; GSM2046575 GEO; GSM2046576 GEO; GSM2046577 GEO; GSM2046578 GEO; GSM2046579 GEO; GSM2046580 GEO; GSM2046581 GEO; GSM2046582 GEO; GSM2046583 GEO; GSM2046584 GEO; GSM2046585 GEO; GSM2046586 GEO; GSM2046587 GEO; GSM2046588 GEO; GSM2046589 GEO; GSM2046590 GEO; GSM2046591 GEO; GSM2046592 GEO; GSM2046593 GEO; GSM2046594 GEO; GSM2046595 GEO; GSM2046596 GEO; GSM2046597 GEO; GSM2046598 GEO; GSM2046599 GEO; GSM2046600 GEO; GSM2046601 GEO; GSM2046602 GEO; GSM2046603 GEO; GSM2046604 GEO; GSM2046605 GEO; GSM2046606 GEO; GSM2046607 GEO; GSM2095708 GEO; GSM2095709 GEO; GSM2124642 GEO; GSM2136630 GEO; GSM2136631 GEO; GSM2136632 GEO; GSM2136633 GEO; GSM2136634 GEO; GSM2136635 GEO; GSM2176269 GEO; GSM2176270 ICLC; HTL95021 IGRhCellID; MCF7 IZSLER; BS TCL 38 JCRB; JCRB0134 JCRB; NIHS0200 KCB; KCB 200831YJ KCLB; 30022 LINCS_HMS; 50029 LINCS_LDP; LCL-1460 Lonza; 113 MeSH; D061986 NCBI_Iran; C135 NCI-DTP; MCF7 PRIDE; PXD000275 PRIDE; PXD000281 PRIDE; PXD000309 PRIDE; PXD000623 PRIDE; PXD000691 PRIDE; PXD001274 PRIDE; PXD001352 PRIDE; PXD001812 PRIDE; PXD002104 PRIDE; PXD002192 PRIDE; PXD002395 PRIDE; PXD002421 PRIDE; PXD002998 PRIDE; PXD004051 PRIDE; PXD004085 PRIDE; PXD004357 PRIDE; PXD005032 RCB; RCB1904 SKY/M-FISH/CGH; 2814 TKG; TKG 0479 TOKU-E; 2383 TOKU-E; 3748 Wikidata; Q1881253

Originate from Same Individual

CVCL_N481 ! Hs 631.T

Elucidation of the anti-autophagy mechanism of the Legionella effector RavZ using semisynthetic LC3 proteins.

  • Yang A
  • Elife
  • 2017 Apr 11

Autophagy is a conserved cellular process involved in the elimination of proteins and organelles. It is also used to combat infection with pathogenic microbes. The intracellular pathogen Legionella pneumophila manipulates autophagy by delivering the effector protein RavZ to deconjugate Atg8/LC3 proteins coupled to phosphatidylethanolamine (PE) on autophagosomal membranes. To understand how RavZ recognizes and deconjugates LC3-PE, we prepared semisynthetic LC3 proteins and elucidated the structures of the RavZ:LC3 interaction. Semisynthetic LC3 proteins allowed the analysis of structure-function relationships. RavZ extracts LC3-PE from the membrane before deconjugation. RavZ initially recognizes the LC3 molecule on membranes via its N-terminal LC3-interacting region (LIR) motif. The RavZ α3 helix is involved in extraction of the PE moiety and docking of the acyl chains into the lipid-binding site of RavZ that is related in structure to that of the phospholipid transfer protein Sec14. Thus, Legionella has evolved a novel mechanism to specifically evade host autophagy.

A Compendium of RNA-Binding Proteins that Regulate MicroRNA Biogenesis.

  • Treiber T
  • Mol. Cell
  • 2017 Apr 20

During microRNA (miRNA) biogenesis, two endonucleolytic reactions convert stem-loop-structured precursors into mature miRNAs. These processing steps can be posttranscriptionally regulated by RNA-binding proteins (RBPs). Here, we have used a proteomics-based pull-down approach to map and characterize the interactome of a multitude of pre-miRNAs. We identify ∼180 RBPs that interact specifically with distinct pre-miRNAs. For functional validation, we combined RNAi and CRISPR/Cas-mediated knockout experiments to analyze RBP-dependent changes in miRNA levels. Indeed, a large number of the investigated candidates, including splicing factors and other mRNA processing proteins, have effects on miRNA processing. As an example, we show that TRIM71/LIN41 is a potent regulator of miR-29a processing and its inactivation directly affects miR-29a targets. We provide an extended database of RBPs that interact with pre-miRNAs in extracts of different cell types, highlighting a widespread layer of co- and posttranscriptional regulation of miRNA biogenesis.

Lithocholic Acid Hydroxyamide Destabilizes Cyclin D1 and Induces G0/G1 Arrest by Inhibiting Deubiquitinase USP2a.

  • Magiera K
  • Cell Chem Biol
  • 2017 Apr 20

USP2a is a deubiquitinase responsible for stabilization of cyclin D1, a crucial regulator of cell-cycle progression and a proto-oncoprotein overexpressed in numerous cancer types. Here we report that lithocholic acid (LCA) derivatives are inhibitors of USP proteins, including USP2a. The most potent LCA derivative, LCA hydroxyamide (LCAHA), inhibits USP2a, leading to a significant Akt/GSK3β-independent destabilization of cyclin D1, but does not change the expression of p27. This leads to the defects in cell-cycle progression. As a result, LCAHA inhibits the growth of cyclin D1-expressing, but not cyclin D1-negative cells, independently of the p53 status. We show that LCA derivatives may be considered as future therapeutics for the treatment of cyclin D1-addicted p53-expressing and p53-defective cancer types.

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.

TP53 exon-6 truncating mutations produce separation of function isoforms with pro-tumorigenic functions.

  • Shirole NH
  • Elife
  • 2016 Oct 19

TP53 truncating mutations are common in human tumors and are thought to give rise to p53-null alleles. Here, we show that TP53 exon-6 truncating mutations occur at higher than expected frequencies and produce proteins that lack canonical p53 tumor suppressor activities but promote cancer cell proliferation, survival, and metastasis. Functionally and molecularly, these p53 mutants resemble the naturally occurring alternative p53 splice variant, p53-psi. Accordingly, these mutants can localize to the mitochondria where they promote tumor phenotypes by binding and activating the mitochondria inner pore permeability regulator, Cyclophilin D (CypD). Together, our studies reveal that TP53 exon-6 truncating mutations, contrary to current beliefs, act beyond p53 loss to promote tumorigenesis, and could inform the development of strategies to target cancers driven by these prevalent mutations.

Transcription Impacts the Efficiency of mRNA Translation via Co-transcriptional N6-adenosine Methylation.

  • Slobodin B
  • Cell
  • 2017 Apr 6

Transcription and translation are two main pillars of gene expression. Due to the different timings, spots of action, and mechanisms of regulation, these processes are mainly regarded as distinct and generally uncoupled, despite serving a common purpose. Here, we sought for a possible connection between transcription and translation. Employing an unbiased screen of multiple human promoters, we identified a positive effect of TATA box on translation and a general coupling between mRNA expression and translational efficiency. Using a CRISPR-Cas9-mediated approach, genome-wide analyses, and in vitro experiments, we show that the rate of transcription regulates the efficiency of translation. Furthermore, we demonstrate that m6A modification of mRNAs is co-transcriptional and depends upon the dynamics of the transcribing RNAPII. Suboptimal transcription rates lead to elevated m6A content, which may result in reduced translation. This study uncovers a general and widespread link between transcription and translation that is governed by epigenetic modification of mRNAs.

Co-transcriptional R-loops are the main cause of estrogen-induced DNA damage.

  • Stork CT
  • Elife
  • 2016 Aug 23

The hormone estrogen (E2) binds the estrogen receptor to promote transcription of E2-responsive genes in the breast and other tissues. E2 also has links to genomic instability, and elevated E2 levels are tied to breast cancer. Here, we show that E2 stimulation causes a rapid, global increase in the formation of R-loops, co-transcriptional RNA-DNA products, which in some instances have been linked to DNA damage. We show that E2-dependent R-loop formation and breast cancer rearrangements are highly enriched at E2-responsive genomic loci and that E2 induces DNA replication-dependent double-strand breaks (DSBs). Strikingly, many DSBs that accumulate in response to E2 are R-loop dependent. Thus, R-loops resulting from the E2 transcriptional response are a significant source of DNA damage. This work reveals a novel mechanism by which E2 stimulation leads to genomic instability and highlights how transcriptional programs play an important role in shaping the genomic landscape of DNA damage susceptibility.

GLUL Promotes Cell Proliferation in Breast Cancer.

  • Wang Y
  • J. Cell. Biochem.
  • 2017 Aug 28

Glutamate-ammonia ligase (GLUL) belongs to the glutamine synthetase family. It catalyzes the synthesis of glutamine from glutamate and ammonia in an ATP-dependent reaction. Here, we found higher expression of GLUL in the breast cancer patients was associated with larger tumor size and higher level of HER2 expression. In addition, GLUL was heterogeneously expressed in various breast cancer cells. The mRNA and protein expression levels of GLUL in SK-BR-3 cells were obviously higher than that in the other types of breast cancer cells. Results showed GLUL knockdown in SK-BR-3 cells could significantly decrease the proliferation ability. Furthermore, GLUL knockdown markedly inhibited the p38 MAPK and ERK1/ERK2 signaling pathways in SK-BR-3 cells. Thus, GLUL may represent a novel target for selectively inhibiting p38 MAPK and ERK1/ERK2 signaling pathways and the proliferation potential of breast cancer cells. J. Cell. Biochem. 118: 2018-2025, 2017. © 2016 Wiley Periodicals, Inc.

Stable and Potent Selenomab-Drug Conjugates.

  • Li X
  • Cell Chem Biol
  • 2017 Apr 20

Selenomabs are engineered monoclonal antibodies with one or more translationally incorporated selenocysteine residues. The unique reactivity of the selenol group of selenocysteine permits site-specific conjugation of drugs. Compared with other natural and unnatural amino acid and carbohydrate residues that have been used for the generation of site-specific antibody-drug conjugates, selenocysteine is particularly reactive, permitting fast, single-step, and efficient reactions under near physiological conditions. Using a tailored conjugation chemistry, we generated highly stable selenomab-drug conjugates and demonstrated their potency and selectivity in vitro and in vivo. These site-specific antibody-drug conjugates built on a selenocysteine interface revealed broad therapeutic utility in liquid and solid malignancy models.

Substrate specificity of TOR complex 2 is determined by a ubiquitin-fold domain of the Sin1 subunit.

  • Tatebe H
  • Elife
  • 2017 Mar 7

The target of rapamycin (TOR) protein kinase forms multi-subunit TOR complex 1 (TORC1) and TOR complex 2 (TORC2), which exhibit distinct substrate specificities. Sin1 is one of the TORC2-specific subunit essential for phosphorylation and activation of certain AGC-family kinases. Here, we show that Sin1 is dispensable for the catalytic activity of TORC2, but its conserved region in the middle (Sin1CRIM) forms a discrete domain that specifically binds the TORC2 substrate kinases. Sin1CRIM fused to a different TORC2 subunit can recruit the TORC2 substrate Gad8 for phosphorylation even in the sin1 null mutant of fission yeast. The solution structure of Sin1CRIM shows a ubiquitin-like fold with a characteristic acidic loop, which is essential for interaction with the TORC2 substrates. The specific substrate-recognition function is conserved in human Sin1CRIM, which may represent a potential target for novel anticancer drugs that prevent activation of the mTORC2 substrates such as AKT.

Context Specificity in Causal Signaling Networks Revealed by Phosphoprotein Profiling.

  • Hill SM
  • Cell Syst
  • 2017 Jan 25

Signaling networks downstream of receptor tyrosine kinases are among the most extensively studied biological networks, but new approaches are needed to elucidate causal relationships between network components and understand how such relationships are influenced by biological context and disease. Here, we investigate the context specificity of signaling networks within a causal conceptual framework using reverse-phase protein array time-course assays and network analysis approaches. We focus on a well-defined set of signaling proteins profiled under inhibition with five kinase inhibitors in 32 contexts: four breast cancer cell lines (MCF7, UACC812, BT20, and BT549) under eight stimulus conditions. The data, spanning multiple pathways and comprising ∼70,000 phosphoprotein and ∼260,000 protein measurements, provide a wealth of testable, context-specific hypotheses, several of which we experimentally validate. Furthermore, the data provide a unique resource for computational methods development, permitting empirical assessment of causal network learning in a complex, mammalian setting.