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Caki-1

RRID:CVCL_0234

Organism

Homo sapiens

Comments

Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: COSMIC cell lines project. Part of: MD Anderson Cell Lines Project. Part of: NCI-60 cancer cell line panel. From: Memorial Sloan Kettering Cancer Center; New York; USA. Registration: Memorial Sloan Kettering Cancer Center Office of Technology Development; SK1980-534. Doubling time: 36 hours (PubMed=25984343); 39 hours (NCI-DTP); ~40-60 hours (DSMZ). HLA typing: A*23:01,24:02:01; B*35:02,44:03:01; C*04:01:01:01; DPB1*02:01:02,10:01; DQB1*02:02,03; DRB1*07:01,11:04:01 (PubMed=15748285). HLA typing: A*23:01,24:02:01; B*35:02,44:03:01; C*04:01:01:01; DPB1*02:01:02,10:01; DQB1*02:02,03:AF; DRB1*07:01,11:04:01 (IPD-IMGT/HLA; 13865). Microsatellite instability: Stable (MSS) (Sanger). Sequence variation: Heterozygous for RB1 p.Leu98Pro (c.293T>C) (CCLE; Cosmic-CLP). Omics: Array-based CGH. Omics: CNV analysis. Omics: Deep exome analysis. Omics: Deep proteome analysis. Omics: Deep RNAseq analysis. Omics: DNA methylation analysis. Omics: Fluorescence phenotype profiling. Omics: GPI-anchored proteins analysis by proteomics. Omics: lncRNA expression profiling. Omics: Metabolome analysis. Omics: Protein expression by reverse-phase protein arrays. Omics: SNP array analysis. Omics: Transcriptome analysis. Genome ancestry: African=1.09%; Native American=0.91%; East Asian, North=2.59%; East Asian, South=0.47%; South Asian=7.88%; European, North=28.81%; European, South=58.26% (PubMed=30894373). Discontinued: DSMZ; ACC-142. Discontinued: RCB; RCB1985. Discontinued: TKG; TKG 0436. Derived from metastatic site: Skin. DT Created: 04-04-12; Last updated: 06-09-19; Version: 30

Proper Citation

DSMZ Cat# ACC-731, RRID:CVCL_0234

Category

Cancer cell line DT Created: 04-04-12; Last updated: 06-09-19; Version: 30

Sex

DT Created: 04-04-12; Last updated: 06-09-19; Version: 30

Synonyms

CAKI-1, CaKi-1, caki-1, CAKI.1, CAKI 1, CAKI1, Caki1 DT Created: 04-04-12, Last updated: 06-09-19, Version: 30

Vendor

DSMZ

Cat Num

ACC-731

Cross References

BTO; BTO:0003204 CLO; CLO_0002175 CLO; CLO_0002176 EFO; EFO_0002149 MCCL; MCC:0000123 CLDB; cl623 CLDB; cl5175 ArrayExpress; E-MTAB-2770 ArrayExpress; E-MTAB-3610 ATCC; HTB-46 BioSample; SAMN01821541 BioSample; SAMN01821674 BioSample; SAMN03473223 BioSample; SAMN10987640 CCLE; CAKI1_KIDNEY CCRID; 3111C0001CCC000244 CCRID; 3131C0001000700135 Cell_Model_Passport; SIDM00941 ChEMBL-Cells; CHEMBL3307522 ChEMBL-Targets; CHEMBL614067 CLS; 300149/p748_Caki-1 Cosmic; 687940 Cosmic; 801356 Cosmic; 849379 Cosmic; 874611 Cosmic; 875871 Cosmic; 897463 Cosmic; 905963 Cosmic; 974303 Cosmic; 979705 Cosmic; 1044261 Cosmic; 1092594 Cosmic; 1305375 Cosmic; 1312363 Cosmic; 1998436 Cosmic; 2036675 Cosmic; 2301558 Cosmic; 2520632 Cosmic-CLP; 905963 DepMap; ACH-000433 DSMZ; ACC-142 DSMZ; ACC-731 GDSC; 905963 GEO; GSM2147 GEO; GSM50229 GEO; GSM50293 GEO; GSM750816 GEO; GSM799374 GEO; GSM799437 GEO; GSM846288 GEO; GSM886902 GEO; GSM887967 GEO; GSM1153447 GEO; GSM1181288 GEO; GSM1181368 GEO; GSM1669644 GEO; GSM2124663 IARC_TP53; 21041 IGRhCellID; Caki1 IPD-IMGT/HLA; 13865 IZSLER; BS TCL 108 JCRB; JCRB0801 KCB; KCB 200850YJ KCLB; 30046 LiGeA; CCLE_484 LINCS_LDP; LCL-1774 MetaboLights; MTBLS737 NCI-DTP; CAKI-1 PharmacoDB; CAKI1_163_2019 PRIDE; PXD003105 PRIDE; PXD005942 RCB; RCB1985 SKY/M-FISH/CGH; 2790 TKG; TKG 0436 Wikidata; Q54808374 DT Created: 04-04-12; Last updated: 06-09-19; Version: 30

Hierarchy

DT Created: 04-04-12; Last updated: 06-09-19; Version: 30

Originate from Same Individual

DT Created: 04-04-12; Last updated: 06-09-19; Version: 30

Publications that use this research resource

Loss of functional BAP1 augments sensitivity to TRAIL in cancer cells.

  • Kolluri KK
  • Elife
  • 2018 Jan 18

Literature context:


Abstract:

Malignant mesothelioma (MM) is poorly responsive to systemic cytotoxic chemotherapy and invariably fatal. Here we describe a screen of 94 drugs in 15 exome-sequenced MM lines and the discovery of a subset defined by loss of function of the nuclear deubiquitinase BRCA associated protein-1 (BAP1) that demonstrate heightened sensitivity to TRAIL (tumour necrosis factor-related apoptosis-inducing ligand). This association is observed across human early passage MM cultures, mouse xenografts and human tumour explants. We demonstrate that BAP1 deubiquitinase activity and its association with ASXL1 to form the Polycomb repressive deubiquitinase complex (PR-DUB) impacts TRAIL sensitivity implicating transcriptional modulation as an underlying mechanism. Death receptor agonists are well-tolerated anti-cancer agents demonstrating limited therapeutic benefit in trials without a targeting biomarker. We identify BAP1 loss-of-function mutations, which are frequent in MM, as a potential genomic stratification tool for TRAIL sensitivity with immediate and actionable therapeutic implications.

Funding information:
  • Cancer Research UK - A17341()
  • NINDS NIH HHS - R01NS043915(United States)
  • Wellcome - WT097452MA()
  • Wellcome Trust - 106555/Z/14/Z()
  • Wellcome Trust - WT107963AIA()

Long non-coding RNA HOTAIR promotes cell migration by upregulating insulin growth factor-binding protein 2 in renal cell carcinoma.

  • Katayama H
  • Sci Rep
  • 2017 Sep 20

Literature context:


Abstract:

Renal cell carcinoma (RCC) is one of the most lethal urologic cancers. About one-third of RCC patients already have distal metastasis at the time of diagnosis. There is growing evidence that Hox antisense intergenic RNA (HOTAIR) plays essential roles in metastasis in several types of cancers. However, the precise mechanism by which HOTAIR enhances malignancy remains unclear, especially in RCC. Here, we demonstrated that HOTAIR enhances RCC-cell migration by regulating the insulin growth factor-binding protein 2 (IGFBP2) expression. HOTAIR expression in tumors was significantly correlated with nuclear grade, lymph-node metastasis, and lung metastasis. High HOTAIR expression was associated with a poor prognosis in both our dataset and The Cancer Genome Atlas dataset. Migratory capacity was enhanced in RCC cell lines in a HOTAIR-dependent manner. HOTAIR overexpression accelerated tumorigenicity and lung metastasis in immunodeficient mice. Microarray analysis revealed that IGFBP2 expression was upregulated in HOTAIR-overexpressing cells compared with control cells. The enhanced migration activity of HOTAIR-overexpressing cells was attenuated by IGFBP2 knockdown. IGFBP2 and HOTAIR were co-expressed in clinical RCC samples. Our findings suggest that the HOTAIR-IGFBP2 axis plays critical roles in RCC metastasis and may serve as a novel therapeutic target for advanced RCC.