FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2106145103> ?p ?o ?g. }

• W2106145103 abstract "Hypoxia inducible factor 1α (HIF1α) is a transcription factor that regulates adaptation of cells to hypoxic microenvironments, for example inside solid tumors. Stabilization of HIF1α can also occur in normoxic conditions in inflamed tissue or as a result of inactivating mutations in negative regulators of HIF1α. Aberrant overexpression of HIF1α in many different cancers has led to intensive efforts to develop HIF1α targeted therapies. However, the role of HIF1α is still poorly understood in chronic inflammation that predisposes the colon to carcinogenesis. We have previously reported that Hif1α transcription is upregulated and the protein is stabilised in inflammatory lesions which are caused by the non-steroidal anti-inflammatory drug (NSAID) sulindac in the mouse proximal colon. Here we exploited this side effect of long-term sulindac administration to analyse the role of Hif1α in colon inflammation using mice with a Villin cre-induced deletion of Hif1α exon 2 in the intestinal epithelium (Hif1αΔIEC ). We also analysed the effect of sulindac sulfide on the Aryl Hydrocarbon Receptor (AHR) pathway in vitro in colon cancer cells. Most sulindac-treated mice developed visible lesions, resembling the appearance of flat or depressed adenomas in the human colon, surrounded by macroscopically normal mucosa. Hif1αΔIEC mice still developed lesions but they were smaller than in the Hif1α-floxed siblings (Hif1αF/F). Microscopically, Hif1αΔIEC mice had significantly less severe colon inflammation than Hif1αF/F mice. Molecular analysis showed reduced MIF and increased E-cadherin mRNA expression in the colon of sulindac-treated Hif1αΔIEC mice. However, immunohistochemistry analysis revealed a defect of E-cadherin protein expression in sulindac-treated Hif1αΔIEC mice. Sulindac sulfide treatment in vitro upregulated Hif1α, c-JUN and IL8 expression through the AHR pathway. Taken together, Hif1α expression augments inflammation in the proximal colon of sulindac-treated mice and AHR activation by sulindac may lead to the reduction of E-cadherin protein levels through the MAPK pathway." @default.
• W2106145103 created "2016-06-24" @default.
• W2106145103 creator A5008816371 @default.
• W2106145103 creator A5024325932 @default.
• W2106145103 creator A5033797872 @default.
• W2106145103 creator A5035610778 @default.
• W2106145103 creator A5052193733 @default.
• W2106145103 creator A5064156396 @default.
• W2106145103 creator A5065006433 @default.
• W2106145103 creator A5071610019 @default.
• W2106145103 creator A5076136165 @default.
• W2106145103 date "2015-01-01" @default.
• W2106145103 modified "2023-10-18" @default.
• W2106145103 title "HIF1α deficiency reduces colon inflammation in a mouse model of proximal colon cancer" @default.
• W2106145103 cites W1964847767 @default.
• W2106145103 cites W1975665042 @default.
• W2106145103 cites W1979377219 @default.
• W2106145103 cites W1982920345 @default.
• W2106145103 cites W1989538067 @default.
• W2106145103 cites W1990607537 @default.
• W2106145103 cites W2005539293 @default.
• W2106145103 cites W2007880486 @default.
• W2106145103 cites W2010950394 @default.
• W2106145103 cites W2011810742 @default.
• W2106145103 cites W2011910303 @default.
• W2106145103 cites W2018782206 @default.
• W2106145103 cites W2025819729 @default.
• W2106145103 cites W2027115372 @default.
• W2106145103 cites W2036733130 @default.
• W2106145103 cites W2036792438 @default.
• W2106145103 cites W2039412091 @default.
• W2106145103 cites W2046440184 @default.
• W2106145103 cites W2058793136 @default.
• W2106145103 cites W2071895328 @default.
• W2106145103 cites W2082862094 @default.
• W2106145103 cites W2087367170 @default.
• W2106145103 cites W2096460816 @default.
• W2106145103 cites W2096619153 @default.
• W2106145103 cites W2097989455 @default.
• W2106145103 cites W2098972920 @default.
• W2106145103 cites W2099852400 @default.
• W2106145103 cites W2102514614 @default.
• W2106145103 cites W2103409364 @default.
• W2106145103 cites W2109492293 @default.
• W2106145103 cites W2112280924 @default.
• W2106145103 cites W2118276393 @default.
• W2106145103 cites W2130035222 @default.
• W2106145103 cites W2134361367 @default.
• W2106145103 cites W2136496098 @default.
• W2106145103 cites W2140855200 @default.
• W2106145103 cites W2142127071 @default.
• W2106145103 cites W2149472502 @default.
• W2106145103 cites W2155554726 @default.
• W2106145103 cites W2157052021 @default.
• W2106145103 cites W2157404189 @default.
• W2106145103 cites W2160872895 @default.
• W2106145103 cites W2165153403 @default.
• W2106145103 cites W2165523086 @default.
• W2106145103 cites W2165901622 @default.
• W2106145103 cites W2171978272 @default.
• W2106145103 cites W4234288885 @default.
• W2106145103 doi "https://doi.org/10.1242/dmm.019000" @default.
• W2106145103 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4582097" @default.
• W2106145103 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26183215" @default.
• W2106145103 hasPublicationYear "2015" @default.
• W2106145103 type Work @default.
• W2106145103 sameAs 2106145103 @default.
• W2106145103 citedByCount "14" @default.
• W2106145103 countsByYear W21061451032016 @default.
• W2106145103 countsByYear W21061451032018 @default.
• W2106145103 countsByYear W21061451032019 @default.
• W2106145103 countsByYear W21061451032020 @default.
• W2106145103 countsByYear W21061451032021 @default.
• W2106145103 countsByYear W21061451032022 @default.
• W2106145103 crossrefType "journal-article" @default.
• W2106145103 hasAuthorship W2106145103A5008816371 @default.
• W2106145103 hasAuthorship W2106145103A5024325932 @default.
• W2106145103 hasAuthorship W2106145103A5033797872 @default.
• W2106145103 hasAuthorship W2106145103A5035610778 @default.
• W2106145103 hasAuthorship W2106145103A5052193733 @default.
• W2106145103 hasAuthorship W2106145103A5064156396 @default.
• W2106145103 hasAuthorship W2106145103A5065006433 @default.
• W2106145103 hasAuthorship W2106145103A5071610019 @default.
• W2106145103 hasAuthorship W2106145103A5076136165 @default.
• W2106145103 hasBestOaLocation W21061451031 @default.
• W2106145103 hasConcept C104317684 @default.
• W2106145103 hasConcept C121608353 @default.
• W2106145103 hasConcept C126322002 @default.
• W2106145103 hasConcept C127561419 @default.
• W2106145103 hasConcept C142724271 @default.
• W2106145103 hasConcept C178790620 @default.
• W2106145103 hasConcept C185592680 @default.
• W2106145103 hasConcept C203014093 @default.
• W2106145103 hasConcept C204232928 @default.
• W2106145103 hasConcept C2776241388 @default.
• W2106145103 hasConcept C2776914184 @default.
• W2106145103 hasConcept C2778452354 @default.
• W2106145103 hasConcept C2778484676 @default.
• W2106145103 hasConcept C502942594 @default.
• W2106145103 hasConcept C526805850 @default.

• next