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MDA-MB-435S

RRID:CVCL_0622

Organism

Homo sapiens

Comments

Problematic cell line: Contaminated. Parent cell line (MDA-MB-435) has been shown to be a M14 derivative. Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: KuDOS 95 cell line panel. Microsatellite instability: Stable (MSS) (PubMed=12661003). Omics: Array-based CGH. Omics: miRNA expression profiling. Omics: SNP array analysis. Omics: Transcriptome analysis. Derived from metastatic site: Subcutaneous; right buttock.

Proper Citation

BCRJ Cat# 0165, RRID:CVCL_0622

Category

Cancer cell line

Sex

Male

Synonyms

MDA-MB-435s, MDA-MB-435 S, MDA-MB-435-S, MDAMB435S

Vendor

BCRJ

Cat Num

0165

Cross References

BTO; BTO:0003941 CLO; CLO_0007638 CLDB; cl7142 ATCC; HTB-129 BCRJ; 0165 CCLE; MDAMB435S_SKIN CCRID; 3111C0001CCC000015 CCRID; 3131C0001000700036 CCRID; 3142C0001000000052 CLS; 300277/p513_MDA-MB-435S Cosmic; 809237 Cosmic; 871155 Cosmic; 894089 Cosmic; 904381 Cosmic; 1044202 Cosmic; 1046951 Cosmic; 1287922 Cosmic; 1289399 Cosmic; 1523969 Cosmic; 1609477 Cosmic; 2301531 GEO; GSM149983 GEO; GSM149991 GEO; GSM149999 GEO; GSM887298 GEO; GSM888373 GEO; GSM1374657 ICLC; HTL03006 LINCS_HMS; 50030 LINCS_LDP; LCL-1307

Hierarchy

CVCL_0417 ! MDA-MB-435

Publications that use this research resource

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

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.