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HEY A8

RRID:CVCL_8878

Organism

Homo sapiens

Comments

Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: MD Anderson Cell Lines Project. Doubling time: 16 hours (PubMed=25984343). Omics: Deep proteome analysis. Omics: Deep RNAseq analysis. Omics: shRNA library screening. Omics: SNP array analysis. Omics: Protein expression by reverse-phase protein arrays. Omics: Transcriptome analysis. Genome ancestry: African=1.54%; Native American=0%; East Asian, North=2.65%; East Asian, South=0%; South Asian=0%; European, North=62.34%; European, South=33.46% (PubMed=30894373). DT Created: 06-06-12; Last updated: 24-05-19; Version: 13

Proper Citation

RRID:CVCL_8878

Category

Cancer cell line DT Created: 06-06-12; Last updated: 24-05-19; Version: 13

Sex

DT Created: 06-06-12; Last updated: 24-05-19; Version: 13

Synonyms

HEY-A8, Hey-A8, Hey A8, HEYA8, HeyA8 DT Created: 06-06-12, Last updated: 24-05-19, Version: 13

Cross References

ArrayExpress; E-MTAB-2770 CCLE; HEYA8_OVARY Cell_Model_Passport; SIDM01215 Cosmic; 1305329 GEO; GSM851918 GEO; GSM887080 GEO; GSM888150 Wikidata; Q54883213 DT Created: 06-06-12; Last updated: 24-05-19; Version: 13

Hierarchy

DT Created: 06-06-12; Last updated: 24-05-19; Version: 13

Originate from Same Individual

DT Created: 06-06-12; Last updated: 24-05-19; Version: 13

Publications that use this research resource

Small interfering RNAs based on huntingtin trinucleotide repeats are highly toxic to cancer cells.

  • Murmann AE
  • EMBO Rep.
  • 2018 Feb 15

Literature context:


Abstract:

Trinucleotide repeat (TNR) expansions in the genome cause a number of degenerative diseases. A prominent TNR expansion involves the triplet CAG in the huntingtin (HTT) gene responsible for Huntington's disease (HD). Pathology is caused by protein and RNA generated from the TNR regions including small siRNA-sized repeat fragments. An inverse correlation between the length of the repeats in HTT and cancer incidence has been reported for HD patients. We now show that siRNAs based on the CAG TNR are toxic to cancer cells by targeting genes that contain long reverse complementary TNRs in their open reading frames. Of the 60 siRNAs based on the different TNRs, the six members in the CAG/CUG family of related TNRs are the most toxic to both human and mouse cancer cells. siCAG/CUG TNR-based siRNAs induce cell death in vitro in all tested cancer cell lines and slow down tumor growth in a preclinical mouse model of ovarian cancer with no signs of toxicity to the mice. We propose to explore TNR-based siRNAs as a novel form of anticancer reagents.

Funding information:
  • NCI NIH HHS - R01 CA167041()
  • NCI NIH HHS - R01CA127645(United States)
  • NCI NIH HHS - R35 CA197450()
  • NCI NIH HHS - T32 CA009560()
  • NCI NIH HHS - T32 CA070085()

Many si/shRNAs can kill cancer cells by targeting multiple survival genes through an off-target mechanism.

  • Putzbach W
  • Elife
  • 2017 Oct 24

Literature context:


Abstract:

Over 80% of multiple-tested siRNAs and shRNAs targeting CD95 or CD95 ligand (CD95L) induce a form of cell death characterized by simultaneous activation of multiple cell death pathways preferentially killing transformed and cancer stem cells. We now show these si/shRNAs kill cancer cells through canonical RNAi by targeting the 3'UTR of critical survival genes in a unique form of off-target effect we call DISE (death induced by survival gene elimination). Drosha and Dicer-deficient cells, devoid of most miRNAs, are hypersensitive to DISE, suggesting cellular miRNAs protect cells from this form of cell death. By testing 4666 shRNAs derived from the CD95 and CD95L mRNA sequences and an unrelated control gene, Venus, we have identified many toxic sequences - most of them located in the open reading frame of CD95L. We propose that specific toxic RNAi-active sequences present in the genome can kill cancer cells.

Funding information:
  • NCI NIH HHS - R35 CA197450()
  • NCI NIH HHS - R50 CA211271()
  • NCI NIH HHS - T32 CA009560()
  • NCI NIH HHS - T32 CA070085()