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Homo sapiens


Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: COSMIC cell lines project. Part of: JFCR39 cancer cell line panel. Part of: KuDOS 95 cell line panel. Part of: MD Anderson Cell Lines Project. Part of: NCI-60 cancer cell line panel. Part of: NCI-7 clinical proteomics reference material cell line panel. Doubling time: 61 hours (NCI-DTP). HLA typing: A*01:01:01,24:02:01; B*07,39; C*07:02:01,12:03:01; DPB1*02:01:02,04:01; DQB1*05:02:01,06:02; DRB1*15:01:01,16:01:01 (PubMed=15748285). Microsatellite instability: Stable (MSS) (Sanger). Sequence variation: Homozygous for CDKN2A deletion (ATCC). 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: lncRNA expression profiling. Omics: Metabolome analysis. Omics: Protein expression by reverse-phase protein arrays. Omics: Proteome analysis by 2D-DE/MS. Omics: SNP array analysis. Omics: Transcriptome analysis. Genome ancestry: African=0%; Native American=0%; East Asian, North=0.16%; East Asian, South=0.88%; South Asian=1.48%; European, North=65.62%; European, South=31.86% (PubMed=30894373). Discontinued: KCLB; 90226. Derived from sampling site: Pleural effusion. DT Created: 04-04-12; Last updated: 05-07-19; Version: 29

Proper Citation

ATCC Cat# CRL-5826, RRID:CVCL_1544


Cancer cell line DT Created: 04-04-12; Last updated: 05-07-19; Version: 29


DT Created: 04-04-12; Last updated: 05-07-19; Version: 29


NCI.H226, NCI H226, H226, H-226, HUT-226, HUT 226, NCIH226 DT Created: 04-04-12, Last updated: 05-07-19, Version: 29



Cat Num


Cross References

BTO; BTO:0003008 CLO; CLO_0008068 EFO; EFO_0002285 AddexBio; C0016011/4916 ArrayExpress; E-MTAB-2706 ArrayExpress; E-MTAB-2770 ArrayExpress; E-MTAB-3610 ATCC; CRL-5826 BioSample; SAMN03471987 BioSample; SAMN10987668 CCLE; NCIH226_LUNG CCRID; 3131C0001001200016 CCRID; 3142C0001000000966 Cell_Model_Passport; SIDM00139 ChEMBL-Cells; CHEMBL3307697 ChEMBL-Targets; CHEMBL614740 Cosmic; 733816 Cosmic; 875850 Cosmic; 877259 Cosmic; 877402 Cosmic; 886388 Cosmic; 903570 Cosmic; 905941 Cosmic; 931374 Cosmic; 974291 Cosmic; 980961 Cosmic; 1006539 Cosmic; 1028953 Cosmic; 1032433 Cosmic; 1047100 Cosmic; 1092618 Cosmic; 1152497 Cosmic; 1175863 Cosmic; 1188585 Cosmic; 1219111 Cosmic; 1239951 Cosmic; 1305346 Cosmic; 1312331 Cosmic; 1436011 Cosmic; 1481544 Cosmic; 1802319 Cosmic; 1870270 Cosmic; 1963326 Cosmic; 1995565 Cosmic; 1998460 Cosmic; 2060522 Cosmic; 2560228 Cosmic; 2664122 Cosmic-CLP; 905941 DepMap; ACH-000367 ENCODE; ENCBS328RVB ENCODE; ENCBS986NWY GDSC; 905941 GEO; GSM2123 GEO; GSM50213 GEO; GSM50276 GEO; GSM62965 GEO; GSM206486 GEO; GSM274785 GEO; GSM274821 GEO; GSM750820 GEO; GSM794278 GEO; GSM799340 GEO; GSM799403 GEO; GSM847074 GEO; GSM844641 GEO; GSM844640 GEO; GSM844642 GEO; GSM887416 GEO; GSM888495 GEO; GSM1153411 GEO; GSM1181351 GEO; GSM1374728 GEO; GSM1374729 GEO; GSM1374730 GEO; GSM1670227 GEO; GSM2124673 IGRhCellID; NCIH226 KCLB; 90226 LiGeA; CCLE_131 LINCS_LDP; LCL-1597 Lonza; 839 NCI-DTP; NCI-H226 PRIDE; PXD005942 SKY/M-FISH/CGH; 2802 Wikidata; Q54907948 DT Created: 04-04-12; Last updated: 05-07-19; Version: 29


DT Created: 04-04-12; Last updated: 05-07-19; Version: 29

Originate from Same Individual

DT Created: 04-04-12; Last updated: 05-07-19; Version: 29

The GSK3 Signaling Axis Regulates Adaptive Glutamine Metabolism in Lung Squamous Cell Carcinoma.

  • Momcilovic M
  • Cancer Cell
  • 2018 May 14

Literature context:


Altered metabolism is a hallmark of cancer growth, forming the conceptual basis for development of metabolic therapies as cancer treatments. We performed in vivo metabolic profiling and molecular analysis of lung squamous cell carcinoma (SCC) to identify metabolic nodes for therapeutic targeting. Lung SCCs adapt to chronic mTOR inhibition and suppression of glycolysis through the GSK3α/β signaling pathway, which upregulates glutaminolysis. Phospho-GSK3α/β protein levels are predictive of response to single-therapy mTOR inhibition while combinatorial treatment with the glutaminase inhibitor CB-839 effectively overcomes therapy resistance. In addition, we identified a conserved metabolic signature in a broad spectrum of hypermetabolic human tumors that may be predictive of patient outcome and response to combined metabolic therapies targeting mTOR and glutaminase.

Funding information:
  • NIAMS NIH HHS - R01 AR061567(United States)

GPR68 Senses Flow and Is Essential for Vascular Physiology.

  • Xu J
  • Cell
  • 2018 Apr 19

Literature context:


Mechanotransduction plays a crucial role in vascular biology. One example of this is the local regulation of vascular resistance via flow-mediated dilation (FMD). Impairment of this process is a hallmark of endothelial dysfunction and a precursor to a wide array of vascular diseases, such as hypertension and atherosclerosis. Yet the molecules responsible for sensing flow (shear stress) within endothelial cells remain largely unknown. We designed a 384-well screening system that applies shear stress on cultured cells. We identified a mechanosensitive cell line that exhibits shear stress-activated calcium transients, screened a focused RNAi library, and identified GPR68 as necessary and sufficient for shear stress responses. GPR68 is expressed in endothelial cells of small-diameter (resistance) arteries. Importantly, Gpr68-deficient mice display markedly impaired acute FMD and chronic flow-mediated outward remodeling in mesenteric arterioles. Therefore, GPR68 is an essential flow sensor in arteriolar endothelium and is a critical signaling component in cardiovascular pathophysiology.

Funding information:
  • NCI NIH HHS - U24 CA126543(United States)

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

  • Kolluri KK
  • Elife
  • 2018 Jan 18

Literature context:


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()

A Predictive Model for Selective Targeting of the Warburg Effect through GAPDH Inhibition with a Natural Product.

  • Liberti MV
  • Cell Metab.
  • 2017 Oct 3

Literature context:


Targeted cancer therapies that use genetics are successful, but principles for selectively targeting tumor metabolism that is also dependent on the environment remain unknown. We now show that differences in rate-controlling enzymes during the Warburg effect (WE), the most prominent hallmark of cancer cell metabolism, can be used to predict a response to targeting glucose metabolism. We establish a natural product, koningic acid (KA), to be a selective inhibitor of GAPDH, an enzyme we characterize to have differential control properties over metabolism during the WE. With machine learning and integrated pharmacogenomics and metabolomics, we demonstrate that KA efficacy is not determined by the status of individual genes, but by the quantitative extent of the WE, leading to a therapeutic window in vivo. Thus, the basis of targeting the WE can be encoded by molecular principles that extend beyond the status of individual genes.

Funding information:
  • NCI NIH HHS - R00 CA168997()
  • NCI NIH HHS - R01 CA174643()
  • NCI NIH HHS - R01 CA193256()
  • NIDDK NIH HHS - R01 DK105550()
  • NIGMS NIH HHS - T32 GM007273()
  • NIGMS NIH HHS - T32 GM008500()

Environmental cystine drives glutamine anaplerosis and sensitizes cancer cells to glutaminase inhibition.

  • Muir A
  • Elife
  • 2017 Aug 15

Literature context:


Many mammalian cancer cell lines depend on glutamine as a major tri-carboxylic acid (TCA) cycle anaplerotic substrate to support proliferation. However, some cell lines that depend on glutamine anaplerosis in culture rely less on glutamine catabolism to proliferate in vivo. We sought to understand the environmental differences that cause differential dependence on glutamine for anaplerosis. We find that cells cultured in adult bovine serum, which better reflects nutrients available to cells in vivo, exhibit decreased glutamine catabolism and reduced reliance on glutamine anaplerosis compared to cells cultured in standard tissue culture conditions. We find that levels of a single nutrient, cystine, accounts for the differential dependence on glutamine in these different environmental contexts. Further, we show that cystine levels dictate glutamine dependence via the cystine/glutamate antiporter xCT/SLC7A11. Thus, xCT/SLC7A11 expression, in conjunction with environmental cystine, is necessary and sufficient to increase glutamine catabolism, defining important determinants of glutamine anaplerosis and glutaminase dependence in cancer.