FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1998174102> ?p ?o ?g. }

• W1998174102 endingPage "7906" @default.
• W1998174102 startingPage "7896" @default.
• W1998174102 abstract "We previously showed that depletion of the retinoblastoma protein (RB) induces down-regulation of the adhesion molecule E-cadherin and thereby triggers the epithelial-mesenchymal transition. To further characterize the effect of RB inactivation on the phenotype of cancer cells, we have now examined RB expression in human breast cancer cell lines and clinical specimens. We found that RB-inactive cells exhibit a mesenchymal-like morphology and are highly invasive. We also found that ZEB proteins, transcriptional repressors of the E-cadherin gene, are markedly up-regulated in these cells in a manner sensitive to the miR-200 family of microRNAs. Moreover, depletion of ZEB in RB-inactive cells suppressed cell invasiveness and proliferation and induced epithelial marker expression. These results implicate ZEB in induction of the epithelial-mesenchymal transition, as well as in maintenance of the mesenchymal phenotype in RB-inactive cells. We also developed a screening program for inhibitors of ZEB1 expression and thereby identified several cyclin-dependent kinase inhibitors that blocked both ZEB1 expression and RB phosphorylation. Together, our findings suggest that RB inactivation contributes to tumor progression not only through loss of cell cycle control but also through up-regulation of ZEB expression and induction of an invasive phenotype. We previously showed that depletion of the retinoblastoma protein (RB) induces down-regulation of the adhesion molecule E-cadherin and thereby triggers the epithelial-mesenchymal transition. To further characterize the effect of RB inactivation on the phenotype of cancer cells, we have now examined RB expression in human breast cancer cell lines and clinical specimens. We found that RB-inactive cells exhibit a mesenchymal-like morphology and are highly invasive. We also found that ZEB proteins, transcriptional repressors of the E-cadherin gene, are markedly up-regulated in these cells in a manner sensitive to the miR-200 family of microRNAs. Moreover, depletion of ZEB in RB-inactive cells suppressed cell invasiveness and proliferation and induced epithelial marker expression. These results implicate ZEB in induction of the epithelial-mesenchymal transition, as well as in maintenance of the mesenchymal phenotype in RB-inactive cells. We also developed a screening program for inhibitors of ZEB1 expression and thereby identified several cyclin-dependent kinase inhibitors that blocked both ZEB1 expression and RB phosphorylation. Together, our findings suggest that RB inactivation contributes to tumor progression not only through loss of cell cycle control but also through up-regulation of ZEB expression and induction of an invasive phenotype." @default.
• W1998174102 created "2016-06-24" @default.
• W1998174102 creator A5010612803 @default.
• W1998174102 creator A5023504370 @default.
• W1998174102 creator A5031414489 @default.
• W1998174102 creator A5039137137 @default.
• W1998174102 creator A5047997260 @default.
• W1998174102 creator A5051962951 @default.
• W1998174102 creator A5054256781 @default.
• W1998174102 creator A5056573153 @default.
• W1998174102 creator A5058280372 @default.
• W1998174102 creator A5063303934 @default.
• W1998174102 creator A5084140379 @default.
• W1998174102 creator A5091499529 @default.
• W1998174102 date "2012-03-01" @default.
• W1998174102 modified "2023-10-17" @default.
• W1998174102 title "Induction of ZEB Proteins by Inactivation of RB Protein Is Key Determinant of Mesenchymal Phenotype of Breast Cancer" @default.
• W1998174102 cites W1971303929 @default.
• W1998174102 cites W1971624340 @default.
• W1998174102 cites W1976324983 @default.
• W1998174102 cites W1978636216 @default.
• W1998174102 cites W1979403925 @default.
• W1998174102 cites W2004000621 @default.
• W1998174102 cites W2030194693 @default.
• W1998174102 cites W2036008499 @default.
• W1998174102 cites W2036647671 @default.
• W1998174102 cites W2043797012 @default.
• W1998174102 cites W2047372188 @default.
• W1998174102 cites W2055395862 @default.
• W1998174102 cites W2073792103 @default.
• W1998174102 cites W2076583198 @default.
• W1998174102 cites W2087367170 @default.
• W1998174102 cites W2101136328 @default.
• W1998174102 cites W2112666597 @default.
• W1998174102 cites W2125120607 @default.
• W1998174102 cites W2128824325 @default.
• W1998174102 cites W2140618607 @default.
• W1998174102 cites W2143825101 @default.
• W1998174102 cites W2155131748 @default.
• W1998174102 cites W2156734818 @default.
• W1998174102 cites W2165901622 @default.
• W1998174102 doi "https://doi.org/10.1074/jbc.m111.313759" @default.
• W1998174102 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3318741" @default.
• W1998174102 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22262832" @default.
• W1998174102 hasPublicationYear "2012" @default.
• W1998174102 type Work @default.
• W1998174102 sameAs 1998174102 @default.
• W1998174102 citedByCount "64" @default.
• W1998174102 countsByYear W19981741022012 @default.
• W1998174102 countsByYear W19981741022013 @default.
• W1998174102 countsByYear W19981741022014 @default.
• W1998174102 countsByYear W19981741022015 @default.
• W1998174102 countsByYear W19981741022016 @default.
• W1998174102 countsByYear W19981741022017 @default.
• W1998174102 countsByYear W19981741022018 @default.
• W1998174102 countsByYear W19981741022019 @default.
• W1998174102 countsByYear W19981741022020 @default.
• W1998174102 countsByYear W19981741022021 @default.
• W1998174102 countsByYear W19981741022022 @default.
• W1998174102 crossrefType "journal-article" @default.
• W1998174102 hasAuthorship W1998174102A5010612803 @default.
• W1998174102 hasAuthorship W1998174102A5023504370 @default.
• W1998174102 hasAuthorship W1998174102A5031414489 @default.
• W1998174102 hasAuthorship W1998174102A5039137137 @default.
• W1998174102 hasAuthorship W1998174102A5047997260 @default.
• W1998174102 hasAuthorship W1998174102A5051962951 @default.
• W1998174102 hasAuthorship W1998174102A5054256781 @default.
• W1998174102 hasAuthorship W1998174102A5056573153 @default.
• W1998174102 hasAuthorship W1998174102A5058280372 @default.
• W1998174102 hasAuthorship W1998174102A5063303934 @default.
• W1998174102 hasAuthorship W1998174102A5084140379 @default.
• W1998174102 hasAuthorship W1998174102A5091499529 @default.
• W1998174102 hasBestOaLocation W19981741021 @default.
• W1998174102 hasConcept C104317684 @default.
• W1998174102 hasConcept C121608353 @default.
• W1998174102 hasConcept C127716648 @default.
• W1998174102 hasConcept C1491633281 @default.
• W1998174102 hasConcept C149402561 @default.
• W1998174102 hasConcept C153911025 @default.
• W1998174102 hasConcept C198826908 @default.
• W1998174102 hasConcept C199835354 @default.
• W1998174102 hasConcept C2776062698 @default.
• W1998174102 hasConcept C2776577112 @default.
• W1998174102 hasConcept C2779013556 @default.
• W1998174102 hasConcept C29537977 @default.
• W1998174102 hasConcept C502942594 @default.
• W1998174102 hasConcept C54355233 @default.
• W1998174102 hasConcept C76419328 @default.
• W1998174102 hasConcept C86803240 @default.
• W1998174102 hasConcept C95444343 @default.
• W1998174102 hasConcept C96232424 @default.
• W1998174102 hasConceptScore W1998174102C104317684 @default.
• W1998174102 hasConceptScore W1998174102C121608353 @default.
• W1998174102 hasConceptScore W1998174102C127716648 @default.
• W1998174102 hasConceptScore W1998174102C1491633281 @default.
• W1998174102 hasConceptScore W1998174102C149402561 @default.
• W1998174102 hasConceptScore W1998174102C153911025 @default.
• W1998174102 hasConceptScore W1998174102C198826908 @default.

• next