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Homo sapiens


Part of: MD Anderson Cell Lines Project. From: Immuno-Biological Laboratories (IBL); Tokyo; Japan. Sequence variation: EGFR p.Glu746_Ala750del (PubMed=17332333). Omics: Deep membrane proteome analysis. Omics: Deep phosphoproteome analysis. Omics: Deep RNAseq analysis. Omics: Protein expression by reverse-phase protein arrays. Omics: SNP array analysis. Omics: Transcriptome analysis.

Proper Citation

BCRJ Cat# 0331, RRID:CVCL_B260


Cancer cell line




PC9, PC-9/S1, PC-9S1



Cat Num


Cross References

BTO; BTO:0005518 CLO; CLO_0050067 EFO; EFO_0002847 BCRJ; 0331 BioSample; SAMN03470946 ChEMBL-Cells; CHEMBL3307867 ChEMBL-Targets; CHEMBL614102 Cosmic; 713867 Cosmic; 801574 Cosmic; 876137 Cosmic; 897746 Cosmic; 911753 Cosmic; 915329 Cosmic; 917985 Cosmic; 929156 Cosmic; 946058 Cosmic; 1001658 Cosmic; 1002731 Cosmic; 1047092 Cosmic; 1128254 Cosmic; 1146943 Cosmic; 1239896 Cosmic; 1336875 Cosmic; 1571735 Cosmic; 1656893 Cosmic; 1731370 Cosmic; 1745414 Cosmic; 2015224 Cosmic; 2125285 ENCODE; ENCBS177ANS ENCODE; ENCBS480XRH ENCODE; ENCBS761VSF ENCODE; ENCBS987JQH GEO; GSM434290 GEO; GSM481160 GEO; GSM784274 GEO; GSM794406 GEO; GSM827407 GEO; GSM1374821 IGRhCellID; PC9GEO LINCS_HMS; 50038 LINCS_LDP; LCL-1630 PRIDE; PXD001548 PRIDE; PXD002224 RCB; RCB4455

Publications that use this research resource

Complement Component 3 Adapts the Cerebrospinal Fluid for Leptomeningeal Metastasis.

  • Boire A
  • Cell
  • 2017 Mar 9

Literature context: oan MassaguéMalladi et al., 2016PC9 ParentalLaboratory of Joan MassaguéNguye


We molecularly dissected leptomeningeal metastasis, or spread of cancer to the cerebrospinal fluid (CSF), which is a frequent and fatal condition mediated by unknown mechanisms. We selected lung and breast cancer cell lines for the ability to infiltrate and grow in CSF, a remarkably acellular, mitogen-poor metastasis microenvironment. Complement component 3 (C3) was upregulated in four leptomeningeal metastatic models and proved necessary for cancer growth within the leptomeningeal space. In human disease, cancer cells within the CSF produced C3 in correlation with clinical course. C3 expression in primary tumors was predictive of leptomeningeal relapse. Mechanistically, we found that cancer-cell-derived C3 activates the C3a receptor in the choroid plexus epithelium to disrupt the blood-CSF barrier. This effect allows plasma components, including amphiregulin, and other mitogens to enter the CSF and promote cancer cell growth. Pharmacologic interference with C3 signaling proved therapeutically beneficial in suppressing leptomeningeal metastasis in these preclinical models.

Funding information:
  • NCI NIH HHS - P01 CA129243()
  • NCI NIH HHS - P30 CA008748()
  • NCI NIH HHS - U54 CA163167()

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: The PC9 (RRID:CVCL_B260) cell line


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()