Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.




Homo sapiens


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). Sequence variation: Heterozygous for BRAF p.Val600Glu (from parent cell line). Sequence variation: Heterozygous for TP53 p.Gly266Glu (from parent cell line). Omics: Array-based CGH. Omics: miRNA expression profiling. Omics: SNP array analysis. Omics: Transcriptome analysis. Derived from metastatic site: Subcutaneous; right buttock.

Proper Citation

ATCC Cat# HTB-129, RRID:CVCL_0622


Cancer cell line




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



Cat Num


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


CVCL_0417 ! MDA-MB-435

Publications that use this research resource

Focal Adhesion- and IGF1R-Dependent Survival and Migratory Pathways Mediate Tumor Resistance to mTORC1/2 Inhibition.

  • Yoon SO
  • Mol. Cell
  • 2017 Aug 3

Literature context: 30A375ATCCCRL-1619MDA-MB-435ATCCHTB-129SK-MEL-19Dr. Paul B. ChapmanN/AS


Aberrant signaling by the mammalian target of rapamycin (mTOR) contributes to the devastating features of cancer cells. Thus, mTOR is a critical therapeutic target and catalytic inhibitors are being investigated as anti-cancer drugs. Although mTOR inhibitors initially block cell proliferation, cell viability and migration in some cancer cells are quickly restored. Despite sustained inhibition of mTORC1/2 signaling, Akt, a kinase regulating cell survival and migration, regains phosphorylation at its regulatory sites. Mechanistically, mTORC1/2 inhibition promotes reorganization of integrin/focal adhesion kinase-mediated adhesomes, induction of IGFR/IR-dependent PI3K activation, and Akt phosphorylation via an integrin/FAK/IGFR-dependent process. This resistance mechanism contributes to xenograft tumor cell growth, which is prevented with mTOR plus IGFR inhibitors, supporting this combination as a therapeutic approach for cancers.

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

Literature context: 35S (RRID:CVCL_0622) and NCI-H


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.

Funding information:
  • NCI NIH HHS - P01 CA129243()
  • NCI NIH HHS - P30 CA045508()