FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2588414287> ?p ?o ?g. }

• W2588414287 endingPage "3717" @default.
• W2588414287 startingPage "3706" @default.
• W2588414287 abstract "Epithelial-mesenchymal transition (EMT) is an important biological process that has been implicated in cancer metastasis. Epithelial cell adhesion molecule (EpCAM) is expressed at the basolateral membrane of most normal epithelial cells but is overexpressed in many epithelial cancers. In our studies on the role of EpCAM in cancer biology, we observed that EpCAM expression is decreased in mesenchymal-like primary cancer specimens in vivo and following induction of EMT in cancer cell lines in vitro. Extracellular signal-related kinase (ERK) is a key regulator of EMT. We observed that EpCAM expression is decreased with activation of the ERK pathway in primary cancer specimens in vivo and in cancer cell lines in vitro. In experimental models, growth factor stimulation and/or oncogene-induced ERK2 activation suppressed EpCAM expression, whereas genetic or pharmacological inhibition of the ERK pathway restored EpCAM expression. In detailed studies of the EpCAM promoter region, we observed that ERK2 suppresses EpCAM transcription directly by binding to a consensus ERK2-binding site in the EpCAM promoter and indirectly through activation of EMT-associated transcription factors SNAI1, SNAI2, TWIST1 and ZEB1, which bind to E-box sites in the EpCAM promoter. Surprisingly, EpCAM appears to modulate ERK activity. Using multiple cell lines, we demonstrated that specific ablation of EpCAM resulted in increased ERK pathway activity and SNAI2 expression, migration and invasion, whereas forced expression of EpCAM resulted in decreased ERK pathway activity and SNAI2 expression, migration and invasion. These observations provide important insights into the regulation of EpCAM expression during EMT, demonstrate an unexpected role for EpCAM in the regulation of ERK and define a novel double-negative feedback loop between EpCAM and ERK that contributes to the regulation of EMT. These studies have important translational implications as both EpCAM and ERK are currently being targeted in human clinical trials." @default.
• W2588414287 created "2017-02-24" @default.
• W2588414287 creator A5004593862 @default.
• W2588414287 creator A5008456176 @default.
• W2588414287 creator A5061892063 @default.
• W2588414287 creator A5062867029 @default.
• W2588414287 creator A5078908482 @default.
• W2588414287 date "2017-02-13" @default.
• W2588414287 modified "2023-09-25" @default.
• W2588414287 title "A double-negative feedback loop between EpCAM and ERK contributes to the regulation of epithelial–mesenchymal transition in cancer" @default.
• W2588414287 cites W1497663772 @default.
• W2588414287 cites W1574811228 @default.
• W2588414287 cites W1775309324 @default.
• W2588414287 cites W1804495077 @default.
• W2588414287 cites W1964081206 @default.
• W2588414287 cites W1964847767 @default.
• W2588414287 cites W1967135832 @default.
• W2588414287 cites W1968897776 @default.
• W2588414287 cites W1970226848 @default.
• W2588414287 cites W1973426525 @default.
• W2588414287 cites W1984484474 @default.
• W2588414287 cites W1986418370 @default.
• W2588414287 cites W1986978780 @default.
• W2588414287 cites W1988134165 @default.
• W2588414287 cites W1989554701 @default.
• W2588414287 cites W1994231692 @default.
• W2588414287 cites W2006644883 @default.
• W2588414287 cites W2012117840 @default.
• W2588414287 cites W2014691022 @default.
• W2588414287 cites W2028593825 @default.
• W2588414287 cites W2033893825 @default.
• W2588414287 cites W2042198997 @default.
• W2588414287 cites W2042965279 @default.
• W2588414287 cites W2051541007 @default.
• W2588414287 cites W2055380229 @default.
• W2588414287 cites W2058763255 @default.
• W2588414287 cites W2059562044 @default.
• W2588414287 cites W2069266255 @default.
• W2588414287 cites W2075705110 @default.
• W2588414287 cites W2078825790 @default.
• W2588414287 cites W2080765801 @default.
• W2588414287 cites W2083307291 @default.
• W2588414287 cites W2098513996 @default.
• W2588414287 cites W2099750732 @default.
• W2588414287 cites W2101136328 @default.
• W2588414287 cites W2102514614 @default.
• W2588414287 cites W2106292881 @default.
• W2588414287 cites W2107552318 @default.
• W2588414287 cites W2111316083 @default.
• W2588414287 cites W2111976640 @default.
• W2588414287 cites W2112666597 @default.
• W2588414287 cites W2115891953 @default.
• W2588414287 cites W2124156632 @default.
• W2588414287 cites W2124358769 @default.
• W2588414287 cites W2128445526 @default.
• W2588414287 cites W2130164253 @default.
• W2588414287 cites W2137143355 @default.
• W2588414287 cites W2142351815 @default.
• W2588414287 cites W2142426658 @default.
• W2588414287 cites W2145533919 @default.
• W2588414287 cites W2150322923 @default.
• W2588414287 cites W2153076514 @default.
• W2588414287 cites W2154185968 @default.
• W2588414287 cites W2157923000 @default.
• W2588414287 cites W2158741313 @default.
• W2588414287 cites W2161028192 @default.
• W2588414287 cites W2165286055 @default.
• W2588414287 cites W2169105660 @default.
• W2588414287 cites W2172224583 @default.
• W2588414287 doi "https://doi.org/10.1038/onc.2016.504" @default.
• W2588414287 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5571977" @default.
• W2588414287 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28192403" @default.
• W2588414287 hasPublicationYear "2017" @default.
• W2588414287 type Work @default.
• W2588414287 sameAs 2588414287 @default.
• W2588414287 citedByCount "47" @default.
• W2588414287 countsByYear W25884142872017 @default.
• W2588414287 countsByYear W25884142872018 @default.
• W2588414287 countsByYear W25884142872019 @default.
• W2588414287 countsByYear W25884142872020 @default.
• W2588414287 countsByYear W25884142872021 @default.
• W2588414287 countsByYear W25884142872022 @default.
• W2588414287 countsByYear W25884142872023 @default.
• W2588414287 crossrefType "journal-article" @default.
• W2588414287 hasAuthorship W2588414287A5004593862 @default.
• W2588414287 hasAuthorship W2588414287A5008456176 @default.
• W2588414287 hasAuthorship W2588414287A5061892063 @default.
• W2588414287 hasAuthorship W2588414287A5062867029 @default.
• W2588414287 hasAuthorship W2588414287A5078908482 @default.
• W2588414287 hasBestOaLocation W25884142872 @default.
• W2588414287 hasConcept C104317684 @default.
• W2588414287 hasConcept C121608353 @default.
• W2588414287 hasConcept C153911025 @default.
• W2588414287 hasConcept C16224149 @default.
• W2588414287 hasConcept C2776677690 @default.
• W2588414287 hasConcept C2779013556 @default.
• W2588414287 hasConcept C2781018059 @default.
• W2588414287 hasConcept C29537977 @default.

• next