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Divergent Ewing's sarcoma EWS/ETS fusions confer a common tumorigenic phenotype on NIH3T3 cells.
Oncogene. 1999 Sep 30; 18(40):5506-13.O

Abstract

Ewing's sarcomas express chimeric transcription factors resulting from a fusion of the amino terminus of the EWS gene to the carboxyl terminus of one of five ETS proteins. While the majority of tumors express EWS/FLI1 fusions, some Ewing's tumors contain variant chimeras such as EWS/ETV1 that have divergent ETS DNA-binding domains. In spite of their structural differences, both EWS/ETS fusions up regulate EAT-2, a previously described EWS/FLI1 target gene. In contrast to EWS/FLI1, NIH3T3 cells expressing EWS/ETV1 cannot form colonies in soft agar though coexpression of a dominant negative truncated ETV1 construct attenuates EWS/FLI1 mediated anchorage independent growth. When EWS/ETV1 or EWS/FLI1 expressing NIH3T3 cells are injected into SCID mice, tumors form more often and faster than with NIH-3T3 cells with empty vector controls. The tumorigenic potency of each EWS/ETS fusion is linked to its C-terminal structure, with the FLI1 C-terminus confering a greater tumorigenic potential than the corresponding ETV1 domain. The resulting EWS/ETV1 and EWS/FLI1 tumors closely resemble each other at both a macroscopic and a microscopic level. These tumors differ greatly from tumors formed by NIH3T3 cells expressing activated RAS. These data indicate that in spite of their structural differences, EWS/ETV1 and EWS/FLI1 promote oncogenesis via similar biologic pathways.

Authors+Show Affiliations

Molecular Biology Institute, Gwynne Hazen Cherry Memorial Labs, University of California at Los Angeles, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10523827

Citation

Thompson, A D., et al. "Divergent Ewing's Sarcoma EWS/ETS Fusions Confer a Common Tumorigenic Phenotype On NIH3T3 Cells." Oncogene, vol. 18, no. 40, 1999, pp. 5506-13.
Thompson AD, Teitell MA, Arvand A, et al. Divergent Ewing's sarcoma EWS/ETS fusions confer a common tumorigenic phenotype on NIH3T3 cells. Oncogene. 1999;18(40):5506-13.
Thompson, A. D., Teitell, M. A., Arvand, A., & Denny, C. T. (1999). Divergent Ewing's sarcoma EWS/ETS fusions confer a common tumorigenic phenotype on NIH3T3 cells. Oncogene, 18(40), 5506-13.
Thompson AD, et al. Divergent Ewing's Sarcoma EWS/ETS Fusions Confer a Common Tumorigenic Phenotype On NIH3T3 Cells. Oncogene. 1999 Sep 30;18(40):5506-13. PubMed PMID: 10523827.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Divergent Ewing's sarcoma EWS/ETS fusions confer a common tumorigenic phenotype on NIH3T3 cells. AU - Thompson,A D, AU - Teitell,M A, AU - Arvand,A, AU - Denny,C T, PY - 1999/10/19/pubmed PY - 1999/10/19/medline PY - 1999/10/19/entrez SP - 5506 EP - 13 JF - Oncogene JO - Oncogene VL - 18 IS - 40 N2 - Ewing's sarcomas express chimeric transcription factors resulting from a fusion of the amino terminus of the EWS gene to the carboxyl terminus of one of five ETS proteins. While the majority of tumors express EWS/FLI1 fusions, some Ewing's tumors contain variant chimeras such as EWS/ETV1 that have divergent ETS DNA-binding domains. In spite of their structural differences, both EWS/ETS fusions up regulate EAT-2, a previously described EWS/FLI1 target gene. In contrast to EWS/FLI1, NIH3T3 cells expressing EWS/ETV1 cannot form colonies in soft agar though coexpression of a dominant negative truncated ETV1 construct attenuates EWS/FLI1 mediated anchorage independent growth. When EWS/ETV1 or EWS/FLI1 expressing NIH3T3 cells are injected into SCID mice, tumors form more often and faster than with NIH-3T3 cells with empty vector controls. The tumorigenic potency of each EWS/ETS fusion is linked to its C-terminal structure, with the FLI1 C-terminus confering a greater tumorigenic potential than the corresponding ETV1 domain. The resulting EWS/ETV1 and EWS/FLI1 tumors closely resemble each other at both a macroscopic and a microscopic level. These tumors differ greatly from tumors formed by NIH3T3 cells expressing activated RAS. These data indicate that in spite of their structural differences, EWS/ETV1 and EWS/FLI1 promote oncogenesis via similar biologic pathways. SN - 0950-9232 UR - https://www.unboundmedicine.com/medline/citation/10523827/Divergent_Ewing's_sarcoma_EWS/ETS_fusions_confer_a_common_tumorigenic_phenotype_on_NIH3T3_cells_ L2 - https://doi.org/10.1038/sj.onc.1202928 DB - PRIME DP - Unbound Medicine ER -