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CAL-51

RRID:CVCL_1110

Organism

Homo sapiens

Comments

Group: Triple negative breast cancer (TNBC) cell line. Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: COSMIC cell lines project. Part of: KuDOS 95 cell line panel. Part of: MD Anderson Cell Lines Project. Doubling time: 24 hours (PubMed=25984343); ~50-60 hours (DSMZ). Microsatellite instability: Instable (MSI-low) (PubMed=12661003; PubMed=15677628; Sanger). Omics: CNV analysis. Omics: Deep exome analysis. Omics: Deep RNAseq analysis. Omics: DNA methylation analysis. Omics: Protein expression by reverse-phase protein arrays. Omics: shRNA library screening. Omics: SNP array analysis. Omics: Transcriptome analysis. Misspelling: Ca151; In Cosmic 1057761. Derived from metastatic site: Pleural effusion.

Proper Citation

DSMZ Cat# ACC-302, RRID:CVCL_1110

Category

Cancer cell line

Sex

Female

Synonyms

CAL 51, CAL51, Cal51, Centre Antoine Lacassagne-51

Vendor

DSMZ

Cat Num

ACC-302

Cross References

BTO; BTO:0000945 CLO; CLO_0002185 EFO; EFO_0005358 ArrayExpress; E-MTAB-2706 ArrayExpress; E-MTAB-2770 ArrayExpress; E-MTAB-3610 BioSample; SAMN03473159 CCLE; CAL51_BREAST ChEMBL-Cells; CHEMBL3308717 ChEMBL-Targets; CHEMBL1075411 Cosmic; 687467 Cosmic; 910927 Cosmic; 1057761 Cosmic; 2164986 Cosmic-CLP; 910927 DSMZ; ACC-302 GDSC; 910927 GEO; GSM115099 GEO; GSM217567 GEO; GSM274645 GEO; GSM274646 GEO; GSM344362 GEO; GSM344412 GEO; GSM350521 GEO; GSM459702 GEO; GSM783973 GEO; GSM827162 GEO; GSM847246 GEO; GSM847456 GEO; GSM886909 GEO; GSM887975 GEO; GSM1172946 GEO; GSM1374429 GEO; GSM1664565 GEO; GSM1669652 IGRhCellID; CAL51 LINCS_HMS; 50008 LINCS_LDP; LCL-1472 Lonza; 1002 PRIDE; PXD000953 Wikidata; Q54808406

Publications that use this research resource

MELK expression correlates with tumor mitotic activity but is not required for cancer growth.

  • Giuliano CJ
  • Elife
  • 2018 Feb 8

Literature context: Dr. Todd Waldman RRID:CVCL_1110


Abstract:

The Maternal Embryonic Leucine Zipper Kinase (MELK) has been identified as a promising therapeutic target in multiple cancer types. MELK over-expression is associated with aggressive disease, and MELK has been implicated in numerous cancer-related processes, including chemotherapy resistance, stem cell renewal, and tumor growth. Previously, we established that triple-negative breast cancer cell lines harboring CRISPR/Cas9-induced null mutations in MELK proliferate at wild-type levels in vitro (Lin et al., 2017). Here, we generate several additional knockout clones of MELK and demonstrate that across cancer types, cells lacking MELK exhibit wild-type growth in vitro, under environmental stress, in the presence of cytotoxic chemotherapies, and in vivo. By combining our MELK-knockout clones with a recently described, highly specific MELK inhibitor, we further demonstrate that the acute inhibition of MELK results in no specific anti-proliferative phenotype. Analysis of gene expression data from cohorts of cancer patients identifies MELK expression as a correlate of tumor mitotic activity, explaining its association with poor clinical prognosis. In total, our results demonstrate the power of CRISPR/Cas9-based genetic approaches to investigate cancer drug targets, and call into question the rationale for treating patients with anti-MELK monotherapies.

Funding information:
  • NIDDK NIH HHS - R01 DK088718(United States)
  • NIH Office of the Director - 1DP5OD021385()