FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2000454318> ?p ?o ?g. }

• W2000454318 abstract "Lysophosphatidic acid (LPA) acts through G-protein coupled transmembrane receptors, and at least 6 types of LPA receptors (LPARs) have been identified. They regulate many different cellular responses, such as proliferation, survival, differentiation, migration, cytoskeletal changes and calcium influx through these pathways, and may act as a positive or negative regulator of cancer cell behaviors in a receptor specific manner which depends on cell types. Gene expression profiles analyzed in rat sarcoma model showed highly metastatic osteosarcoma cells expressing abundant LPA receptor-3 (LPAR3) compared to mesenchymal stem cells and non-metastatic MFH cells. In the current study, we generated LPAR3-knockdown cells from human fibrosarcoma HT1080 and osteosarcoma HOS cells by transfection with shRNA plasmids and investigated the involvement of LPA3 pathway for cell migration and invasion abilities. Both sarcoma cells expressed through LPAR1 to 5 except for LPAR1 in osteosarcoma HOS. Firstly, we tested the effects of chemical inhibitors of downstream effector of G-proteins, and results suggested that downstream of Gi and Gq protein inhibition suppressed cell motility in both sarcoma cells, while downstream of G12/13 inhibition did not. Then, we generated LPAR3 knockdown cells by transfection of shRNA for LPAR3, which resulted in effective knockdown of the LPAR3 expression in those cells. Expression of autotaxin, a mediator for LPA production, was suppressed in HT1080 but not in HOS by shRNA, indicating the difference of LPA production loop between those cells. LPAR3 knockdown did not affect cellular growth rates in both sarcoma cells. Moreover, LPA treatments stimulated cell proliferation in a dose dependent manner even in LPAR-3 knockdown cells, suggesting that LPA signaling on cell proliferation could be regulated by other LPAR pathways rather than LPAR3 in these cells. On the contrary, LPAR3-knockdown cells showed significantly lower cell motility than control cells both in cell motility assay and in scrape assay. Invasion assay with the Matrigel-coated filter also showed significantly lower invasion activities in LPAR3-knockdown HT1080 cells, which originally showed strong invasive capacity. While, there were no differences observed in matrix metalloproteinase (MMP) -2 and 9 activities on gelatin zymography, suggesting that the control of invasiveness through LPAR3 signaling pathways was independently regulated from MMPs. These results suggest that a part of the abilities for cell migration and invasion in human sarcoma cells were possibly regulated through the downstream of LPAR3, Gi and Gq protein signaling pathways, and those pathways could be the candidates for molecular targeted therapy against sarcomas. Further elucidation of detailed mechanisms underlying in these complex pathways will be required for future therapeutic approach. Citation Format: Kanya Honoki, Hiromasa Tsujiuchi, Akira Kido, Shinji Tsukamoto, Yasuhito Tanaka, Toshifumi Tsujiuchi. Lysophosphatidic acid receptor-3 pathways are involved in up-regulation of cell migration and invasion activity of human sarcoma cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3775. doi:10.1158/1538-7445.AM2013-3775" @default.
• W2000454318 created "2016-06-24" @default.
• W2000454318 creator A5002870764 @default.
• W2000454318 creator A5026197189 @default.
• W2000454318 creator A5040534370 @default.
• W2000454318 creator A5051406303 @default.
• W2000454318 creator A5082187394 @default.
• W2000454318 creator A5088612923 @default.
• W2000454318 date "2013-04-15" @default.
• W2000454318 modified "2023-09-25" @default.
• W2000454318 title "Abstract 3775: Lysophosphatidic acid receptor-3 pathways are involved in up-regulation of cell migration and invasion activity of human sarcoma cells." @default.
• W2000454318 doi "https://doi.org/10.1158/1538-7445.am2013-3775" @default.
• W2000454318 hasPublicationYear "2013" @default.
• W2000454318 type Work @default.
• W2000454318 sameAs 2000454318 @default.
• W2000454318 citedByCount "0" @default.
• W2000454318 crossrefType "proceedings-article" @default.
• W2000454318 hasAuthorship W2000454318A5002870764 @default.
• W2000454318 hasAuthorship W2000454318A5026197189 @default.
• W2000454318 hasAuthorship W2000454318A5040534370 @default.
• W2000454318 hasAuthorship W2000454318A5051406303 @default.
• W2000454318 hasAuthorship W2000454318A5082187394 @default.
• W2000454318 hasAuthorship W2000454318A5088612923 @default.
• W2000454318 hasConcept C126322002 @default.
• W2000454318 hasConcept C137738243 @default.
• W2000454318 hasConcept C1491633281 @default.
• W2000454318 hasConcept C170493617 @default.
• W2000454318 hasConcept C173396325 @default.
• W2000454318 hasConcept C185592680 @default.
• W2000454318 hasConcept C190232843 @default.
• W2000454318 hasConcept C2776661833 @default.
• W2000454318 hasConcept C2777751087 @default.
• W2000454318 hasConcept C3020616263 @default.
• W2000454318 hasConcept C502942594 @default.
• W2000454318 hasConcept C54009773 @default.
• W2000454318 hasConcept C54355233 @default.
• W2000454318 hasConcept C62112901 @default.
• W2000454318 hasConcept C71924100 @default.
• W2000454318 hasConcept C81885089 @default.
• W2000454318 hasConcept C86803240 @default.
• W2000454318 hasConcept C95444343 @default.
• W2000454318 hasConceptScore W2000454318C126322002 @default.
• W2000454318 hasConceptScore W2000454318C137738243 @default.
• W2000454318 hasConceptScore W2000454318C1491633281 @default.
• W2000454318 hasConceptScore W2000454318C170493617 @default.
• W2000454318 hasConceptScore W2000454318C173396325 @default.
• W2000454318 hasConceptScore W2000454318C185592680 @default.
• W2000454318 hasConceptScore W2000454318C190232843 @default.
• W2000454318 hasConceptScore W2000454318C2776661833 @default.
• W2000454318 hasConceptScore W2000454318C2777751087 @default.
• W2000454318 hasConceptScore W2000454318C3020616263 @default.
• W2000454318 hasConceptScore W2000454318C502942594 @default.
• W2000454318 hasConceptScore W2000454318C54009773 @default.
• W2000454318 hasConceptScore W2000454318C54355233 @default.
• W2000454318 hasConceptScore W2000454318C62112901 @default.
• W2000454318 hasConceptScore W2000454318C71924100 @default.
• W2000454318 hasConceptScore W2000454318C81885089 @default.
• W2000454318 hasConceptScore W2000454318C86803240 @default.
• W2000454318 hasConceptScore W2000454318C95444343 @default.
• W2000454318 hasLocation W20004543181 @default.
• W2000454318 hasOpenAccess W2000454318 @default.
• W2000454318 hasPrimaryLocation W20004543181 @default.
• W2000454318 hasRelatedWork W1967162674 @default.
• W2000454318 hasRelatedWork W1978548948 @default.
• W2000454318 hasRelatedWork W1982898420 @default.
• W2000454318 hasRelatedWork W1991037807 @default.
• W2000454318 hasRelatedWork W1992452415 @default.
• W2000454318 hasRelatedWork W2011148925 @default.
• W2000454318 hasRelatedWork W2065352766 @default.
• W2000454318 hasRelatedWork W2065492096 @default.
• W2000454318 hasRelatedWork W2090598533 @default.
• W2000454318 hasRelatedWork W2231721598 @default.
• W2000454318 hasRelatedWork W2259367957 @default.
• W2000454318 hasRelatedWork W2283791313 @default.
• W2000454318 hasRelatedWork W2338154782 @default.
• W2000454318 hasRelatedWork W2464767256 @default.
• W2000454318 hasRelatedWork W2563385190 @default.
• W2000454318 hasRelatedWork W2581210979 @default.
• W2000454318 hasRelatedWork W2586434761 @default.
• W2000454318 hasRelatedWork W2802670193 @default.
• W2000454318 hasRelatedWork W2808683307 @default.
• W2000454318 hasRelatedWork W2971476141 @default.
• W2000454318 isParatext "false" @default.
• W2000454318 isRetracted "false" @default.
• W2000454318 magId "2000454318" @default.
• W2000454318 workType "article" @default.