FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3022201908> ?p ?o ?g. }

• W3022201908 abstract "Abstract Studies examining many different cancers have demonstrated that inflammation plays a critical role in tumor progression, in part through the release of proteases from stromal cells that function to either remodel the tumor microenvironment or to directly stimulate cancer cells to grow. One specific protease, neutrophil elastase (NE), has been shown to be a critical regulator of cancer growth in several mouse models. Accordingly, our laboratory demonstrated that NE, most likely from granulocytic myeloid-derived suppressor cells, potentially promotes prostate cancer progression in several different in-vivo and in-vitro models. To date, however, little is known regarding the mechanisms utilized by NE to promote tumor growth. It has been suggested that NE might cleave epidermal growth factor (EGF) or transforming growth factor-α from the cell surface to induce activation of EGFR/ERK signal transduction in an autocrine fashion. Alternatively, NE has been shown to enter into early endosomes to degrade insulin receptor substrate-I, ultimately resulting in phosphoinositol 3-kinase hyperactivity and subsequent tumor cell proliferation. Here we demonstrate that NE triggered proliferative signals in six prostate cell lines representing the spectrum of prostate cell differentiation, including normal prostatic epithelium, benign prostatic hypertrophy, and metastatic prostate cancer. Focusing on ERK signaling, we found that the stimulatory effect of NE on ERK phosphorylation was dose dependent and was abrogated by small interfering RNA induced EGFR knockdown, as well as by pretreatment of cells with irreversible EGFR inhibitor AG1478. Unlike EGF, however, NE-initiated EGFR phosphorylation was minimal. Thus, while EGFR appears to be critical for NE-induced ERK activation, perhaps it is not extensively activated directly by NE. Notably, discoidin domain receptor-1 (DDR1) was strongly expressed in normal prostate epithelium cells, but gradually decreased and had little expression in benign and metastatic prostate cancer cells sequentially. Nevertheless, similar to EGFR knockdown, silencing of DDR1 in all cell types inhibited NE mediated pERK upregulation, suggesting that DDR1 may also be important for NE-induced action. Together, our data suggest that NE, in concert with low level signals from the EGFR and DDR1, play an important role in promoting prostate cell proliferation both in normal and cancerous prostate epithelial cells." @default.
• W3022201908 created "2020-05-13" @default.
• W3022201908 creator A5006107046 @default.
• W3022201908 creator A5039728337 @default.
• W3022201908 creator A5050369503 @default.
• W3022201908 date "2020-04-01" @default.
• W3022201908 modified "2023-10-16" @default.
• W3022201908 title "SAT-138 Neutrophil Elastase Promotes Proliferative Signals in Prostate Cells Through EGFR and DDR1" @default.
• W3022201908 doi "https://doi.org/10.1210/jendso/bvaa046.1405" @default.
• W3022201908 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7208048" @default.
• W3022201908 hasPublicationYear "2020" @default.
• W3022201908 type Work @default.
• W3022201908 sameAs 3022201908 @default.
• W3022201908 citedByCount "0" @default.
• W3022201908 crossrefType "journal-article" @default.
• W3022201908 hasAuthorship W3022201908A5006107046 @default.
• W3022201908 hasAuthorship W3022201908A5039728337 @default.
• W3022201908 hasAuthorship W3022201908A5050369503 @default.
• W3022201908 hasBestOaLocation W30222019081 @default.
• W3022201908 hasConcept C121608353 @default.
• W3022201908 hasConcept C126322002 @default.
• W3022201908 hasConcept C128240485 @default.
• W3022201908 hasConcept C16930146 @default.
• W3022201908 hasConcept C170493617 @default.
• W3022201908 hasConcept C185592680 @default.
• W3022201908 hasConcept C2776107976 @default.
• W3022201908 hasConcept C2776362946 @default.
• W3022201908 hasConcept C2776438761 @default.
• W3022201908 hasConcept C2779438470 @default.
• W3022201908 hasConcept C2779723316 @default.
• W3022201908 hasConcept C2780192828 @default.
• W3022201908 hasConcept C3020616263 @default.
• W3022201908 hasConcept C502942594 @default.
• W3022201908 hasConcept C54355233 @default.
• W3022201908 hasConcept C57074206 @default.
• W3022201908 hasConcept C62112901 @default.
• W3022201908 hasConcept C62478195 @default.
• W3022201908 hasConcept C71924100 @default.
• W3022201908 hasConcept C7876069 @default.
• W3022201908 hasConcept C81885089 @default.
• W3022201908 hasConcept C86803240 @default.
• W3022201908 hasConcept C95444343 @default.
• W3022201908 hasConceptScore W3022201908C121608353 @default.
• W3022201908 hasConceptScore W3022201908C126322002 @default.
• W3022201908 hasConceptScore W3022201908C128240485 @default.
• W3022201908 hasConceptScore W3022201908C16930146 @default.
• W3022201908 hasConceptScore W3022201908C170493617 @default.
• W3022201908 hasConceptScore W3022201908C185592680 @default.
• W3022201908 hasConceptScore W3022201908C2776107976 @default.
• W3022201908 hasConceptScore W3022201908C2776362946 @default.
• W3022201908 hasConceptScore W3022201908C2776438761 @default.
• W3022201908 hasConceptScore W3022201908C2779438470 @default.
• W3022201908 hasConceptScore W3022201908C2779723316 @default.
• W3022201908 hasConceptScore W3022201908C2780192828 @default.
• W3022201908 hasConceptScore W3022201908C3020616263 @default.
• W3022201908 hasConceptScore W3022201908C502942594 @default.
• W3022201908 hasConceptScore W3022201908C54355233 @default.
• W3022201908 hasConceptScore W3022201908C57074206 @default.
• W3022201908 hasConceptScore W3022201908C62112901 @default.
• W3022201908 hasConceptScore W3022201908C62478195 @default.
• W3022201908 hasConceptScore W3022201908C71924100 @default.
• W3022201908 hasConceptScore W3022201908C7876069 @default.
• W3022201908 hasConceptScore W3022201908C81885089 @default.
• W3022201908 hasConceptScore W3022201908C86803240 @default.
• W3022201908 hasConceptScore W3022201908C95444343 @default.
• W3022201908 hasLocation W30222019081 @default.
• W3022201908 hasLocation W30222019082 @default.
• W3022201908 hasOpenAccess W3022201908 @default.
• W3022201908 hasPrimaryLocation W30222019081 @default.
• W3022201908 hasRelatedWork W1118369 @default.
• W3022201908 hasRelatedWork W17662013 @default.
• W3022201908 hasRelatedWork W21064940 @default.
• W3022201908 hasRelatedWork W21323388 @default.
• W3022201908 hasRelatedWork W22038449 @default.
• W3022201908 hasRelatedWork W2856950 @default.
• W3022201908 hasRelatedWork W3189568 @default.
• W3022201908 hasRelatedWork W371148 @default.
• W3022201908 hasRelatedWork W4913624 @default.
• W3022201908 hasRelatedWork W5219062 @default.
• W3022201908 isParatext "false" @default.
• W3022201908 isRetracted "false" @default.
• W3022201908 magId "3022201908" @default.
• W3022201908 workType "article" @default.