FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2233685125> ?p ?o ?g. }

• W2233685125 endingPage "884" @default.
• W2233685125 startingPage "884" @default.
• W2233685125 abstract "Proc Amer Assoc Cancer Res, Volume 47, 20063758 Epidermal growth factor receptor (EGFR)/HER1 is expressed at high levels in ∼20% of breast cancers and correlates with poor disease prognosis. One mechanism that contributes to the generation and maintenance of cancerous cells is the disruption of the cellular cytoskeleton. Microtubule associated proteins (MAPs) are major components of cytoskeleton proteins associated with microtubule assembly and its stabilization. MAP-2, a component of the MAP family, is a marker for neurons and its immunoreactivity has been demonstrated in several neoplasms. We hypothesized that MAP-2 expression is deregulated in EGFR overexpressing breast cancers thus rendering them resistant to conventional therapy. Here we show that loss of MAP-2 expression in breast cancer cells during sustained activation of the EGFR results in resistance to chemotherapeutic drugs. We first evaluated the expression of MAP-2 in a range of breast cancer cells and found that all cell lines expressed varying degrees of MAP-2. However when compared on the basis of their EGFR status, we observed higher expression of MAP-2 in EGFR overexpressing cells than in non-EGFR overexpressing cells both at protein and mRNA levels. To investigate whether the expression of MAP-2 is regulated by the expression of EGFR we selected two cell lines based on their responsiveness to EGF. MCF-7 and MCF-10A cells were challenged with increasing doses of EGF (25-150 ng/ml) and examined for the expression of phosphorylated EGFR. We observed that MCF-7 cells were weakly and MCF-10A cells were strongly stimulated when challenged by increasing doses of EGF. We next examined the expression of MAP-2 in cell lines challenged with EGF and observed that although MAP-2 expression increased with increasing doses of EGF, its expression was almost completely lost at concentrations >100 ng/ml of EGF treatment. This observation suggested a possible mechanism of resistance in breast cancer patients with EGFR overexpression. Based on these observations we conclude that with constant EGF stimulation, cells lose their MAP-2 expression that is required for microtubule stabilization and subsequent cell cycle arrest. In next series of experiments we sought to understand how MAP-2 expression would change in EGFR expressing cells that are challenged with EGF and then treated with microtubule disrupting agents. We found increasing resistance to growth inhibition by docetaxel in cells that were challenged with higher concentrations of EGFR (>50 ng/ml). This suggested that over expression of EGFR signaling in breast cancers could, in fact, be responsible for resistance to therapeutic agents. The loss of MAP-2 expression could have implications in treatment of breast cancers overexpressing the EGFR and exhibiting resistance to conventional therapy." @default.
• W2233685125 created "2016-06-24" @default.
• W2233685125 creator A5020709165 @default.
• W2233685125 creator A5021336715 @default.
• W2233685125 creator A5045791812 @default.
• W2233685125 creator A5065217156 @default.
• W2233685125 creator A5070638161 @default.
• W2233685125 date "2006-04-15" @default.
• W2233685125 modified "2023-09-23" @default.
• W2233685125 title "Accumulated cyclin B1 by RASSF1A enhances microtubule damaging agent-induced cell death through the mediation of hyperphosphorylated Cdc25C and Cdc2" @default.
• W2233685125 hasPublicationYear "2006" @default.
• W2233685125 type Work @default.
• W2233685125 sameAs 2233685125 @default.
• W2233685125 citedByCount "0" @default.
• W2233685125 crossrefType "journal-article" @default.
• W2233685125 hasAuthorship W2233685125A5020709165 @default.
• W2233685125 hasAuthorship W2233685125A5021336715 @default.
• W2233685125 hasAuthorship W2233685125A5045791812 @default.
• W2233685125 hasAuthorship W2233685125A5065217156 @default.
• W2233685125 hasAuthorship W2233685125A5070638161 @default.
• W2233685125 hasConcept C120504264 @default.
• W2233685125 hasConcept C121608353 @default.
• W2233685125 hasConcept C20418707 @default.
• W2233685125 hasConcept C2777506169 @default.
• W2233685125 hasConcept C2778437423 @default.
• W2233685125 hasConcept C2779438470 @default.
• W2233685125 hasConcept C29537977 @default.
• W2233685125 hasConcept C502942594 @default.
• W2233685125 hasConcept C54355233 @default.
• W2233685125 hasConcept C86803240 @default.
• W2233685125 hasConcept C95444343 @default.
• W2233685125 hasConcept C96232424 @default.
• W2233685125 hasConceptScore W2233685125C120504264 @default.
• W2233685125 hasConceptScore W2233685125C121608353 @default.
• W2233685125 hasConceptScore W2233685125C20418707 @default.
• W2233685125 hasConceptScore W2233685125C2777506169 @default.
• W2233685125 hasConceptScore W2233685125C2778437423 @default.
• W2233685125 hasConceptScore W2233685125C2779438470 @default.
• W2233685125 hasConceptScore W2233685125C29537977 @default.
• W2233685125 hasConceptScore W2233685125C502942594 @default.
• W2233685125 hasConceptScore W2233685125C54355233 @default.
• W2233685125 hasConceptScore W2233685125C86803240 @default.
• W2233685125 hasConceptScore W2233685125C95444343 @default.
• W2233685125 hasConceptScore W2233685125C96232424 @default.
• W2233685125 hasLocation W22336851251 @default.
• W2233685125 hasOpenAccess W2233685125 @default.
• W2233685125 hasPrimaryLocation W22336851251 @default.
• W2233685125 hasRelatedWork W129985875 @default.
• W2233685125 hasRelatedWork W1979162692 @default.
• W2233685125 hasRelatedWork W2013154192 @default.
• W2233685125 hasRelatedWork W2014743208 @default.
• W2233685125 hasRelatedWork W2048890543 @default.
• W2233685125 hasRelatedWork W2052057895 @default.
• W2233685125 hasRelatedWork W2074161849 @default.
• W2233685125 hasRelatedWork W2136715524 @default.
• W2233685125 hasRelatedWork W2219595429 @default.
• W2233685125 hasRelatedWork W2225191199 @default.
• W2233685125 hasRelatedWork W2313411379 @default.
• W2233685125 hasRelatedWork W2321904123 @default.
• W2233685125 hasRelatedWork W2443950890 @default.
• W2233685125 hasRelatedWork W2601052641 @default.
• W2233685125 hasRelatedWork W2739244759 @default.
• W2233685125 hasRelatedWork W2740756479 @default.
• W2233685125 hasRelatedWork W2791781412 @default.
• W2233685125 hasRelatedWork W2968724383 @default.
• W2233685125 hasRelatedWork W3160247579 @default.
• W2233685125 hasRelatedWork W3195720813 @default.
• W2233685125 hasVolume "66" @default.
• W2233685125 isParatext "false" @default.
• W2233685125 isRetracted "false" @default.
• W2233685125 magId "2233685125" @default.
• W2233685125 workType "article" @default.