FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2090836265> ?p ?o ?g. }

• W2090836265 endingPage "4468" @default.
• W2090836265 startingPage "4461" @default.
• W2090836265 abstract "Transforming Growth Factor-b (TGFb) is a major driving force of the Epithelial-to-Mesenchymal (EMT) genetic program, which becomes overactive in the pathophysiology of many age-related human diseases. TGFb-driven EMT is sufficient to generate migrating cancer stem cells by directly linking the acquisition of cellular motility with the maintenance of tumor-initiating (stemness) capacity. Chronic diseases exhibiting excessive fibrosis can be caused by repeated and sustained infliction of TGFb-driven EMT, which increases collagen and extracellular matrix synthesis. Pharmacological prevention and/or reversal of TGFb-induced EMT may therefore have important clinical applications in the management of cancer metastasis as well as in the prevention and/or treatment of end-state organ failures. Earlier studies from our group have revealed that clinically-relevant concentrations of the biguanide derivative metformin, the most widely used oral agent to lower blood glucose concentration in patients with type 2 diabetes and metabolic syndrome, notably decreased both the self-renewal and the proliferation of trastuzumab-refractory breast cancer stem cell populations. Given that: a.) tumor-initiating cancer stem cells display a significant enrichment in the expression of basal/mesenchymal or myoepithelial markers, including an increased secretion of TGFb; b.) metformin treatment impedes the ontogeny of generating the stem cell phenotype by transcriptionally repressing key drivers of the EMT genetic program (e.g. ZEB1, TWIST1, SNAIL2 [Slug], TGFbs), we recently hypothesized that prevention of TGFb-induced EMT might represent a common molecular mechanism underlying the anti-cancer stem cells and anti-fibrotic actions of metformin. Remarkably, metformin exposure not only impedes TGFb-promoted loss of the epithelial marker E-cadherin in MCF-7 breast cancer cells but it prevents further TGF-induced cell scattering and accumulation of the mesenchymal marker vimentin in Madin-Darby canine kidney (MDCK) cells. We now propose that metformin, by weakening the ability of TGFb signaling to fully induce mesenchymal cell states in a variety of pathological processes including fibrosis (e.g. chronic renal disease, non-alcoholic steatohepatitis, heart failure or sclerosis) and malignant progression (and likely by reducing TGFb-regulated inflammation and immune responses -inflamm-aging-), molecularly behaves as a bona fide anti-aging modality." @default.
• W2090836265 created "2016-06-24" @default.
• W2090836265 creator A5014700626 @default.
• W2090836265 creator A5017248208 @default.
• W2090836265 creator A5030166947 @default.
• W2090836265 creator A5040427139 @default.
• W2090836265 creator A5053780005 @default.
• W2090836265 creator A5077187730 @default.
• W2090836265 date "2010-11-15" @default.
• W2090836265 modified "2023-10-18" @default.
• W2090836265 title "Metformin against TGFβ-induced epithelial-to-mesenchymal transition (EMT): From cancer stem cells to aging-associated fibrosis" @default.
• W2090836265 cites W1647673097 @default.
• W2090836265 cites W187284916 @default.
• W2090836265 cites W1982437692 @default.
• W2090836265 cites W1986834354 @default.
• W2090836265 cites W1988782755 @default.
• W2090836265 cites W1994378142 @default.
• W2090836265 cites W2005436781 @default.
• W2090836265 cites W2017277573 @default.
• W2090836265 cites W2025647419 @default.
• W2090836265 cites W2026231752 @default.
• W2090836265 cites W2034022260 @default.
• W2090836265 cites W2043376395 @default.
• W2090836265 cites W2045250251 @default.
• W2090836265 cites W2049102197 @default.
• W2090836265 cites W2053428121 @default.
• W2090836265 cites W2062268212 @default.
• W2090836265 cites W2064176617 @default.
• W2090836265 cites W2066134485 @default.
• W2090836265 cites W2069312908 @default.
• W2090836265 cites W2082603625 @default.
• W2090836265 cites W2099864799 @default.
• W2090836265 cites W2104312647 @default.
• W2090836265 cites W2105480437 @default.
• W2090836265 cites W2105665055 @default.
• W2090836265 cites W2125747634 @default.
• W2090836265 cites W2128910004 @default.
• W2090836265 cites W2139151018 @default.
• W2090836265 cites W2143383125 @default.
• W2090836265 cites W2153193122 @default.
• W2090836265 cites W2155554726 @default.
• W2090836265 cites W2158731007 @default.
• W2090836265 cites W2165469857 @default.
• W2090836265 cites W2165901622 @default.
• W2090836265 cites W2171059311 @default.
• W2090836265 cites W2172083228 @default.
• W2090836265 doi "https://doi.org/10.4161/cc.9.22.14048" @default.
• W2090836265 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21088486" @default.
• W2090836265 hasPublicationYear "2010" @default.
• W2090836265 type Work @default.
• W2090836265 sameAs 2090836265 @default.
• W2090836265 citedByCount "195" @default.
• W2090836265 countsByYear W20908362652012 @default.
• W2090836265 countsByYear W20908362652013 @default.
• W2090836265 countsByYear W20908362652014 @default.
• W2090836265 countsByYear W20908362652015 @default.
• W2090836265 countsByYear W20908362652016 @default.
• W2090836265 countsByYear W20908362652017 @default.
• W2090836265 countsByYear W20908362652018 @default.
• W2090836265 countsByYear W20908362652019 @default.
• W2090836265 countsByYear W20908362652020 @default.
• W2090836265 countsByYear W20908362652021 @default.
• W2090836265 countsByYear W20908362652022 @default.
• W2090836265 countsByYear W20908362652023 @default.
• W2090836265 crossrefType "journal-article" @default.
• W2090836265 hasAuthorship W2090836265A5014700626 @default.
• W2090836265 hasAuthorship W2090836265A5017248208 @default.
• W2090836265 hasAuthorship W2090836265A5030166947 @default.
• W2090836265 hasAuthorship W2090836265A5040427139 @default.
• W2090836265 hasAuthorship W2090836265A5053780005 @default.
• W2090836265 hasAuthorship W2090836265A5077187730 @default.
• W2090836265 hasBestOaLocation W20908362651 @default.
• W2090836265 hasConcept C121608353 @default.
• W2090836265 hasConcept C126322002 @default.
• W2090836265 hasConcept C134018914 @default.
• W2090836265 hasConcept C198826908 @default.
• W2090836265 hasConcept C2777688063 @default.
• W2090836265 hasConcept C2779013556 @default.
• W2090836265 hasConcept C2780323712 @default.
• W2090836265 hasConcept C2780559512 @default.
• W2090836265 hasConcept C28328180 @default.
• W2090836265 hasConcept C502942594 @default.
• W2090836265 hasConcept C54355233 @default.
• W2090836265 hasConcept C55427017 @default.
• W2090836265 hasConcept C555293320 @default.
• W2090836265 hasConcept C71924100 @default.
• W2090836265 hasConcept C76419328 @default.
• W2090836265 hasConcept C86803240 @default.
• W2090836265 hasConcept C95444343 @default.
• W2090836265 hasConceptScore W2090836265C121608353 @default.
• W2090836265 hasConceptScore W2090836265C126322002 @default.
• W2090836265 hasConceptScore W2090836265C134018914 @default.
• W2090836265 hasConceptScore W2090836265C198826908 @default.
• W2090836265 hasConceptScore W2090836265C2777688063 @default.
• W2090836265 hasConceptScore W2090836265C2779013556 @default.
• W2090836265 hasConceptScore W2090836265C2780323712 @default.
• W2090836265 hasConceptScore W2090836265C2780559512 @default.
• W2090836265 hasConceptScore W2090836265C28328180 @default.

• next