FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2495118976> ?p ?o ?g. }

• W2495118976 abstract "Background: Previous studies have shown that epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) treatment in lung cancer can lead to the development of pulmonary fibrosis (PF). In other studies, it has been shown that reduced telomerase reverse transcriptase (TERT) function increases susceptibility to PF. In this work, we hypothesize that TERT is associated with the pathogenesis of EGFR-TKI induced PF via important signaling pathways. Methods: HCC827 cells (EGFR L858R) was treated with gefitinib and TERT expression level was detected following the treatment. To investigate the molecular changes following gefitinib treatment, we also performed a 84-TF qPCR- microarray and a qPCR microarray for 84-key secreted proteins of cytokines and chemokines. The level of interleukin-6(IL-6) was further measured with ELISA in cell medium following the gefitinib treatment. Fibrogenic markers were detected after co-culturing HCC827 with lung fibroblast IMR-90 cells. Results: TERT gene expression was significantly decreased over 90% after gefitinib treatment. Early growth response protein 1(EGR-1) and E2F transcription factor 1(E2F1) were significantly down-regulated as major TFs that are responsive to gefitinib treatment. Both EGR-1 and E2F1 have been shown to regulate TERT expression in previous studies. In addition, TFs including JUN and most REL members involved in the NF-κB pathway, were significantly up-regulated after gefitinib treatment, which are known to lead to the activation of the senescence-associated secretory phenotype (SASP) pathway. IL-6 mRNA as well as protein secretion were both significantly up-regulated after gefitinib treatment. After co-culturing HCC827 and IMR-90 for 7 days and treating with gefitinib, the growth of IMR-90 cells were increased compare to the control group. Fibrogenic markers, e.g. COL1A1 (Collagen, Type I, Alpha 1), α-SMA (alpha smooth muscle actin), FSP-1(Fibroblast-specific protein 1), etc. were all up-regulated. Conclusion: Our data suggest that EGFR inhibition leads to lung epithelial cell senescence via inhibiting TERT function and activating of the SASP pathway, which further activates fibroblasts and induces fribrogenesis. Continued studies are warranted to further understand the molecular signaling in this mechanism. Citation Format: Rongrong Wei, Wanqing Liu. EGFR-TERT cooperation in the development of EGFR-TKI treatment induced pulmonary fibrosis. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2851." @default.
• W2495118976 created "2016-08-23" @default.
• W2495118976 creator A5044688218 @default.
• W2495118976 creator A5050664601 @default.
• W2495118976 date "2016-07-15" @default.
• W2495118976 modified "2023-09-27" @default.
• W2495118976 title "Abstract 2851: EGFR-TERT cooperation in the development of EGFR-TKI treatment induced pulmonary fibrosis" @default.
• W2495118976 doi "https://doi.org/10.1158/1538-7445.am2016-2851" @default.
• W2495118976 hasPublicationYear "2016" @default.
• W2495118976 type Work @default.
• W2495118976 sameAs 2495118976 @default.
• W2495118976 citedByCount "0" @default.
• W2495118976 crossrefType "proceedings-article" @default.
• W2495118976 hasAuthorship W2495118976A5044688218 @default.
• W2495118976 hasAuthorship W2495118976A5050664601 @default.
• W2495118976 hasConcept C121608353 @default.
• W2495118976 hasConcept C126322002 @default.
• W2495118976 hasConcept C2776256026 @default.
• W2495118976 hasConcept C2777506169 @default.
• W2495118976 hasConcept C2777930144 @default.
• W2495118976 hasConcept C2779438470 @default.
• W2495118976 hasConcept C2780580887 @default.
• W2495118976 hasConcept C502942594 @default.
• W2495118976 hasConcept C71924100 @default.
• W2495118976 hasConcept C86803240 @default.
• W2495118976 hasConceptScore W2495118976C121608353 @default.
• W2495118976 hasConceptScore W2495118976C126322002 @default.
• W2495118976 hasConceptScore W2495118976C2776256026 @default.
• W2495118976 hasConceptScore W2495118976C2777506169 @default.
• W2495118976 hasConceptScore W2495118976C2777930144 @default.
• W2495118976 hasConceptScore W2495118976C2779438470 @default.
• W2495118976 hasConceptScore W2495118976C2780580887 @default.
• W2495118976 hasConceptScore W2495118976C502942594 @default.
• W2495118976 hasConceptScore W2495118976C71924100 @default.
• W2495118976 hasConceptScore W2495118976C86803240 @default.
• W2495118976 hasLocation W24951189761 @default.
• W2495118976 hasOpenAccess W2495118976 @default.
• W2495118976 hasPrimaryLocation W24951189761 @default.
• W2495118976 hasRelatedWork W1543661498 @default.
• W2495118976 hasRelatedWork W1616413320 @default.
• W2495118976 hasRelatedWork W2005757044 @default.
• W2495118976 hasRelatedWork W2014743208 @default.
• W2495118976 hasRelatedWork W2080019448 @default.
• W2495118976 hasRelatedWork W2136715524 @default.
• W2495118976 hasRelatedWork W2165707701 @default.
• W2495118976 hasRelatedWork W2740276727 @default.
• W2495118976 hasRelatedWork W2770640950 @default.
• W2495118976 hasRelatedWork W2790904046 @default.
• W2495118976 hasRelatedWork W2795384223 @default.
• W2495118976 hasRelatedWork W2800083469 @default.
• W2495118976 hasRelatedWork W2888679980 @default.
• W2495118976 hasRelatedWork W2902322225 @default.
• W2495118976 hasRelatedWork W2913109827 @default.
• W2495118976 hasRelatedWork W2954393543 @default.
• W2495118976 hasRelatedWork W2963540928 @default.
• W2495118976 hasRelatedWork W3014128096 @default.
• W2495118976 hasRelatedWork W3015809074 @default.
• W2495118976 hasRelatedWork W3118115295 @default.
• W2495118976 isParatext "false" @default.
• W2495118976 isRetracted "false" @default.
• W2495118976 magId "2495118976" @default.
• W2495118976 workType "article" @default.