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HT-1080

RRID:CVCL_0317

Organism

Homo sapiens

Comments

Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: COSMIC cell lines project. Part of: ENCODE project common cell types; tier 3. Part of: MD Anderson Cell Lines Project. Part of: Naval Biosciences Laboratory (NBL) collection (transferred to ATCC in 1982). Doubling time: 26 hours (PubMed=4132053); ~30 hours (DSMZ). Microsatellite instability: Stable (MSS) (Sanger). Sequence variation: Homozygous for CDKN2A deletion (ATCC). Sequence variation: Heterozygous for IDH1 p.Arg132Cys (c.394C>T) (PubMed=26368816). Sequence variation: Heterozygous for NRAS p.Gln61Lys (c.181C>A) (ATCC; PubMed=12068308). Omics: Deep exome analysis. Omics: Deep RNAseq analysis. Omics: DNA methylation analysis. Omics: Protein expression by reverse-phase protein arrays. Omics: SNP array analysis. Omics: Transcriptome analysis. Genome ancestry: African=0.86%; Native American=0.35%; East Asian, North=1.36%; East Asian, South=0.29%; South Asian=0%; European, North=68.21%; European, South=28.94% (PubMed=30894373). Misspelling: HT1180; Occasionally. Discontinued: ATCC; CRL-7951. Discontinued: RCB; RCB1956. DT Created: 04-04-12; Last updated: 24-05-19; Version: 29

Proper Citation

RCB Cat# RCB1956, RRID:CVCL_0317

Category

Cancer cell line DT Created: 04-04-12; Last updated: 24-05-19; Version: 29

Sex

DT Created: 04-04-12; Last updated: 24-05-19; Version: 29

Synonyms

Ht-1080, HT 1080, HT1080, HT 1080.T DT Created: 04-04-12, Last updated: 24-05-19, Version: 29

Vendor

RCB

Cat Num

RCB1956

Cross References

BTO; BTO:0001282 CLO; CLO_0004266 CLO; CLO_0004276 EFO; EFO_0002059 MCCL; MCC:0000210 CLDB; cl1735 CLDB; cl1736 CLDB; cl1737 CLDB; cl1738 CLDB; cl1740 CLDB; cl1741 CLDB; cl1742 CLDB; cl4913 ArrayExpress; E-MTAB-2706 ArrayExpress; E-MTAB-2770 ArrayExpress; E-MTAB-3610 ATCC; CCL-121 ATCC; CRL-7951 BCRC; 60037 BCRJ; 0110 BioSample; SAMN01821563 BioSample; SAMN01821634 BioSample; SAMN01821685 BioSample; SAMN01821731 BioSample; SAMN03471913 CCLE; HT1080_SOFT_TISSUE CCRID; 3111C0001CCC000070 CCRID; 3142C0001000000116 CCTCC; GDC0105 Cell_Model_Passport; SIDM00828 ChEMBL-Cells; CHEMBL3308396 ChEMBL-Targets; CHEMBL614580 CLS; 300216/p517_HT-1080 Cosmic; 716177 Cosmic; 716188 Cosmic; 724819 Cosmic; 907064 Cosmic; 912000 Cosmic; 1045409 Cosmic; 1067221 Cosmic; 1933190 Cosmic; 2009505 Cosmic; 2301553 Cosmic; 2307731 Cosmic; 2560245 Cosmic-CLP; 907064 DSMZ; ACC-315 ECACC; 85111505 ENCODE; ENCBS039VHD ENCODE; ENCBS225AAA ENCODE; ENCBS512AAA ENCODE; ENCBS513AAA ENCODE; ENCBS617SGR ENCODE; ENCBS688VJF ENCODE; ENCBS798NML ENCODE; ENCBS816VMN ENCODE; ENCBS937RAY GDSC; 907064 GEO; GSM185089 GEO; GSM185090 GEO; GSM256074 GEO; GSM256075 GEO; GSM256076 GEO; GSM256077 GEO; GSM256078 GEO; GSM256079 GEO; GSM256080 GEO; GSM256081 GEO; GSM256082 GEO; GSM256083 GEO; GSM256084 GEO; GSM256085 GEO; GSM256086 GEO; GSM256087 GEO; GSM256088 GEO; GSM256089 GEO; GSM256090 GEO; GSM256091 GEO; GSM256092 GEO; GSM256093 GEO; GSM256094 GEO; GSM256095 GEO; GSM256096 GEO; GSM256097 GEO; GSM256098 GEO; GSM256099 GEO; GSM256100 GEO; GSM256101 GEO; GSM256102 GEO; GSM256103 GEO; GSM256104 GEO; GSM256105 GEO; GSM256106 GEO; GSM256107 GEO; GSM256108 GEO; GSM256109 GEO; GSM256110 GEO; GSM256111 GEO; GSM256112 GEO; GSM256113 GEO; GSM256114 GEO; GSM827307 GEO; GSM887136 GEO; GSM888207 GEO; GSM1669908 GEO; GSM1676302 GEO; GSM1701637 IBRC; C10104 ICLC; HTL98016 IGRhCellID; HT1080 IZSLER; BS TCL 27 JCRB; IFO50354 JCRB; JCRB9113 KCB; KCB 2013029YJ KCLB; 10121 LINCS_LDP; LCL-1435 Lonza; 744 NCBI_Iran; C437 RCB; RCB1956 TKG; TKG 0202 TOKU-E; 1963 Wikidata; Q5636047 DT Created: 04-04-12; Last updated: 24-05-19; Version: 29

Hierarchy

DT Created: 04-04-12; Last updated: 24-05-19; Version: 29

Originate from Same Individual

DT Created: 04-04-12; Last updated: 24-05-19; Version: 29

Recognition and ER Quality Control of Misfolded Formylglycine-Generating Enzyme by Protein Disulfide Isomerase.

  • Schlotawa L
  • Cell Rep
  • 2018 Jul 3

Literature context:


Abstract:

Multiple sulfatase deficiency (MSD) is a fatal, inherited lysosomal storage disorder characterized by reduced activities of all sulfatases in patients. Sulfatases require a unique post-translational modification of an active-site cysteine to formylglycine that is catalyzed by the formylglycine-generating enzyme (FGE). FGE mutations that affect intracellular protein stability determine residual enzyme activity and disease severity in MSD patients. Here, we show that protein disulfide isomerase (PDI) plays a pivotal role in the recognition and quality control of MSD-causing FGE variants. Overexpression of PDI reduces the residual activity of unstable FGE variants, whereas inhibition of PDI function rescues the residual activity of sulfatases in MSD fibroblasts. Mass spectrometric analysis of a PDI+FGE variant covalent complex allowed determination of the molecular signature for FGE recognition by PDI. Our findings highlight the role of PDI as a disease modifier in MSD, which may also be relevant for other ER-associated protein folding pathologies.

Funding information:
  • NIAID NIH HHS - 5T32AI007485(United States)

Immunomimetic Designer Cells Protect Mice from MRSA Infection.

  • Liu Y
  • Cell
  • 2018 Jun 12

Literature context:


Abstract:

Many community- and hospital-acquired bacterial infections are caused by antibiotic-resistant pathogens. Methicillin-resistant Staphylococcus aureus (MRSA) predisposes humans to invasive infections that are difficult to eradicate. We designed a closed-loop gene network programming mammalian cells to autonomously detect and eliminate bacterial infections. The genetic circuit contains human Toll-like receptors as the bacterial sensor and a synthetic promoter driving reversible and adjustable expression of lysostaphin, a bacteriolytic enzyme highly lethal to S. aureus. Immunomimetic designer cells harboring this genetic circuit exhibited fast and robust sense-and-destroy kinetics against live staphylococci. When tested in a foreign-body infection model in mice, microencapsulated cell implants prevented planktonic MRSA infection and reduced MRSA biofilm formation by 91%. Notably, this system achieved a 100% cure rate of acute MRSA infections, whereas conventional vancomycin treatment failed. These results suggest that immunomimetic designer cells could offer a therapeutic approach for early detection, prevention, and cure of pathogenic infections in the post-antibiotic era.

Funding information:
  • Biotechnology and Biological Sciences Research Council - BB/J015652/1(United Kingdom)

Detection of proteolytic activity by covalent tethering of fluorogenic substrates in zymogram gels.

  • Deshmukh AA
  • BioTechniques
  • 2018 May 26

Literature context:


Abstract:

Current zymographic techniques detect only a subset of known proteases due to the limited number of native proteins that have been optimized for incorporation into polyacrylamide gels. To address this limitation, we have developed a technique to covalently incorporate fluorescently labeled, protease-sensitive peptides using an azido-PEG3-maleimide crosslinker. Peptides incorporated into gels enabled measurement of MMP-2, -9, -14, and bacterial collagenase. Sensitivity analysis demonstrated that use of peptide functionalized gels could surpass detection limits of current techniques. Finally, electrophoresis of conditioned media from cultured cells resulted in the appearance of several proteolytic bands, some of which were undetectable by gelatin zymography. Taken together, these results demonstrate that covalent incorporation of fluorescent substrates can greatly expand the library of detectable proteases using zymographic techniques.

Funding information:
  • NIDCR NIH HHS - R01 DE19452(United States)

Copper-Binding Small Molecule Induces Oxidative Stress and Cell-Cycle Arrest in Glioblastoma-Patient-Derived Cells.

  • Shimada K
  • Cell Chem Biol
  • 2018 May 17

Literature context:


Abstract:

Transition metals are essential, but deregulation of their metabolism causes toxicity. Here, we report that the compound NSC319726 binds copper to induce oxidative stress and arrest glioblastoma-patient-derived cells at picomolar concentrations. Pharmacogenomic analysis suggested that NSC319726 and 65 other structural analogs exhibit lethality through metal binding. Although NSC319726 has been reported to function as a zinc ionophore, we report here that this compound binds to copper to arrest cell growth. We generated and validated pharmacogenomic predictions: copper toxicity was substantially inhibited by hypoxia, through an hypoxia-inducible-factor-1α-dependent pathway; copper-bound NSC319726 induced the generation of reactive oxygen species and depletion of deoxyribosyl purines, resulting in cell-cycle arrest. These results suggest that metal-induced DNA damage may be a consequence of exposure to some xenobiotics, therapeutic agents, as well as other causes of copper dysregulation, and reveal a potent mechanism for targeting glioblastomas.

Funding information:
  • NCI NIH HHS - P01 CA087497()
  • NCI NIH HHS - R35 CA209896()
  • NIAID NIH HHS - R01 AI62261(United States)

GPR68 Senses Flow and Is Essential for Vascular Physiology.

  • Xu J
  • Cell
  • 2018 Apr 19

Literature context:


Abstract:

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)

Shigella entry unveils a calcium/calpain-dependent mechanism for inhibiting sumoylation.

  • Lapaquette P
  • Elife
  • 2017 Dec 12

Literature context:


Abstract:

Disruption of the sumoylation/desumoylation equilibrium is associated with several disease states such as cancer and infections, however the mechanisms regulating the global SUMO balance remain poorly defined. Here, we show that infection by Shigella flexneri, the causative agent of human bacillary dysentery, switches off host sumoylation during epithelial cell infection in vitro and in vivo and that this effect is mainly mediated by a calcium/calpain-induced cleavage of the SUMO E1 enzyme SAE2, thus leading to sumoylation inhibition. Furthermore, we describe a mechanism by which Shigella promotes its own invasion by altering the sumoylation state of RhoGDIα, a master negative regulator of RhoGTPase activity and actin polymerization. Together, our data suggest that SUMO modification is essential to restrain pathogenic bacterial entry by limiting cytoskeletal rearrangement induced by bacterial effectors. Moreover, these findings identify calcium-activated calpains as powerful modulators of cellular sumoylation levels with potentially broad implications in several physiological and pathological situations.

Funding information:
  • NCI NIH HHS - 5 R01CA 140729-02(United States)

Synthesis and anticancer activity of novel quinazolinone-based rhodanines.

  • El-Sayed S
  • Chem Cent J
  • 2017 Oct 13

Literature context:


Abstract:

BACKGROUND: Rhodanines and quinazolinones have been reported to possess various pharmacological activities. RESULTS: A novel series of twenty quinazolinone-based rhodanines were synthesized via Knoevenagel condensation between 4-[3-(substitutedphenyl)-3,4-dihydro-4-oxoquinazolin-2-yl)methoxy]substituted-benzaldehydes and rhodanine. Elemental and spectral analysis were used to confirm structures of the newly synthesized compounds. The newly synthesized compounds were biologically evaluated for in vitro cytotoxic activity against the human fibrosarcoma cell line HT-1080 as a preliminary screen using the MTT assay. CONCLUSIONS: All the target compounds were active, displaying IC50 values roughly in the range of 10-60 µM. Structure-activity relationship study revealed that bulky, hydrophobic, and electron withdrawing substituents at the para-position of the quinazolinone 3-phenyl ring as well as methoxy substitution on the central benzene ring, enhance cytotoxic activity. The four most cytotoxic compounds namely, 45, 43, 47, and 37 were further tested against two human leukemia cell lines namely, HL-60 and K-562 and showed cytotoxic activity in the low micromolar range with compound 45 being the most active, having IC50 values of 1.2 and 1.5 μM, respectively. Interestingly, all four compounds were devoid of cytotoxicity against normal human fibroblasts strain AG01523, indicating that the synthesized rhodanines may be selectively toxic against cancer cells. Mechanistic studies revealed that the most cytotoxic target compounds exhibit pro-apoptotic activity and trigger oxidative stress in cancer cells.

Systematic Quantification of Population Cell Death Kinetics in Mammalian Cells.

  • Forcina GC
  • Cell Syst
  • 2017 Jun 28

Literature context:


Abstract:

Cytotoxic compounds are important drugs and research tools. Here, we introduce a method, scalable time-lapse analysis of cell death kinetics (STACK), to quantify the kinetics of compound-induced cell death in mammalian cells at the population level. STACK uses live and dead cell markers, high-throughput time-lapse imaging, and mathematical modeling to determine the kinetics of population cell death over time. We used STACK to profile the effects of over 1,800 bioactive compounds on cell death in two human cancer cell lines, resulting in a large and freely available dataset. 79 potent lethal compounds common to both cell lines caused cell death with widely divergent kinetics. 13 compounds triggered cell death within hours, including the metallophore zinc pyrithione. Mechanistic studies demonstrated that this rapid onset lethal phenotype was caused in human cancer cells by metabolic disruption and ATP depletion. These results provide the first comprehensive survey of cell death kinetics and analysis of rapid-onset lethal compounds.

Funding information:
  • NCI NIH HHS - R00 CA166517()

Co-option of an endogenous retrovirus envelope for host defense in hominid ancestors.

  • Blanco-Melo D
  • Elife
  • 2017 Apr 11

Literature context:


Abstract:

Endogenous retroviral sequences provide a molecular fossil record of ancient infections whose analysis might illuminate mechanisms of viral extinction. A close relative of gammaretroviruses, HERV-T, circulated in primates for ~25 million years (MY) before apparent extinction within the past ~8 MY. Construction of a near-complete catalog of HERV-T fossils in primate genomes allowed us to estimate a ~32 MY old ancestral sequence and reconstruct a functional envelope protein (ancHTenv) that could support infection of a pseudotyped modern gammaretrovirus. Using ancHTenv, we identify monocarboxylate transporter-1 (MCT-1) as a receptor used by HERV-T for attachment and infection. A single HERV-T provirus in hominid genomes includes an env gene (hsaHTenv) that has been uniquely preserved. This apparently exapted HERV-T env could not support virion infection but could block ancHTenv mediated infection, by causing MCT-1 depletion from cell surfaces. Thus, hsaHTenv may have contributed to HERV-T extinction, and could also potentially regulate cellular metabolism.

Single-Molecule Analysis of mtDNA Replication Uncovers the Basis of the Common Deletion.

  • Phillips AF
  • Mol. Cell
  • 2017 Feb 2

Literature context:


Abstract:

Mutations in mtDNA lead to muscular and neurological diseases and are linked to aging. The most frequent aberrancy is the "common deletion" that involves a 4,977-bp region flanked by 13-bp repeats. To investigate the basis of this deletion, we developed a single-molecule mtDNA combing method. The analysis of replicating mtDNA molecules provided in vivo evidence in support of the asymmetric mode of replication. Furthermore, we observed frequent fork stalling at the junction of the common deletion, suggesting that impaired replication triggers the formation of this toxic lesion. In parallel experiments, we employed mito-TALENs to induce breaks in distinct loci of the mitochondrial genome and found that breaks adjacent to the 5' repeat trigger the common deletion. Interestingly, this process was mediated by the mitochondrial replisome independent of canonical DSB repair. Altogether, our data underscore a unique replication-dependent repair pathway that leads to the mitochondrial common deletion.