FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2114585931> ?p ?o ?g. }

• W2114585931 abstract "Abstract Background Homeodomain-interacting protein kinase-2 (HIPK2), a transcriptional co-repressor with apoptotic function, can affect hypoxia-inducible factor 1 (HIF-1) transcriptional activity, through downmodulation of its HIF-1α subunit, in normoxic condition. Under hypoxia, a condition often found in solid tumors, HIF-1α is activated to induce target genes involved in chemoresistance, inhibition of apoptosis and tumor progression. Here, we investigated whether the HIPK2 overexpression could downregulate HIF-1α expression and activity in tumor cells treated with hypoxia-mimicking condition, and evaluated whether HIPK2-dependent downregulation of HIF-1α could sensitize chemoresistant tumor cells to adriamycin (ADR)-induced apoptosis. Methods Tumor cell lines carrying wild-type p53, siRNA p53, or mutant p53 were overexpressed with HIPK2 (full length or catalytic inactive mutant) and treated with cobalt chloride (CoCl 2 ) to mimic hypoxia, in the presence or absence of ADR treatment. HIF-1α expression was measured by semiquantitative reverse-transcriptase (RT)-PCR and Western immunoblotting and HIF-1 activity was evaluated by luciferase assay using reporter plasmid containing hypoxia response elements (HREs) upstream of luciferase gene. HIF-1 target genes, including multidrug resistance 1 (MDR1) and the antiapoptotic Bcl2 were determined by RT-PCR. Cell survival and apoptosis were measured by colony assay and cleavage of the caspase-3 substrate PARP, respectively. Results Overexpression of HIPK2 resulted in downmodulation of cobalt-stabilized HIF-1α protein and HIF-1α mRNA levels, with subsequent inhibition of HIF-1 transcriptional activity. MDR1 and Bcl-2 gene expression was downmodulated by HIPK2 overexpression in cobalt-treated cells. Inhibition of HIF-1 transcriptional activity was dependent on HIPK2 catalytic activity. HIPK2 overexpression did not induce per se apoptosis of cobalt-treated cells, on the contrary it sensitized cobalt-treated cells to ADR-induced apoptosis, regardless of their p53 status. Conclusion The ability of HIPK2 to restore the apoptosis-inducing potential of chemotherapeutic drug in hypoxia-mimicking condition and therefore to sensitize chemoresistant tumor cells suggests that HIPK2 may induce fundamental alterations in cell signaling pathways, involving or not p53 function. Thus potential use of HIPK2 is promising for cancer treatment by potentiating cytotoxic therapies, regardless of p53 cell status." @default.
• W2114585931 created "2016-06-24" @default.
• W2114585931 creator A5000153354 @default.
• W2114585931 creator A5004148079 @default.
• W2114585931 creator A5008407729 @default.
• W2114585931 creator A5051429563 @default.
• W2114585931 date "2009-01-07" @default.
• W2114585931 modified "2023-10-15" @default.
• W2114585931 title "Inhibition of HIF-1alpha activity by homeodomain-interacting protein kinase-2 correlates with sensitization of chemoresistant cells to undergo apoptosis" @default.
• W2114585931 cites W1937401270 @default.
• W2114585931 cites W1964037605 @default.
• W2114585931 cites W1976880272 @default.
• W2114585931 cites W1990714971 @default.
• W2114585931 cites W1997204305 @default.
• W2114585931 cites W2011810742 @default.
• W2114585931 cites W2028847457 @default.
• W2114585931 cites W2030969771 @default.
• W2114585931 cites W2044774111 @default.
• W2114585931 cites W2048679209 @default.
• W2114585931 cites W2054311839 @default.
• W2114585931 cites W2063822655 @default.
• W2114585931 cites W2069698188 @default.
• W2114585931 cites W2072839085 @default.
• W2114585931 cites W2074582828 @default.
• W2114585931 cites W2085609942 @default.
• W2114585931 cites W2092322149 @default.
• W2114585931 cites W2092677877 @default.
• W2114585931 cites W2092678097 @default.
• W2114585931 cites W2099928427 @default.
• W2114585931 cites W2109803994 @default.
• W2114585931 cites W2109920630 @default.
• W2114585931 cites W2118177072 @default.
• W2114585931 cites W2135397379 @default.
• W2114585931 doi "https://doi.org/10.1186/1476-4598-8-1" @default.
• W2114585931 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2628864" @default.
• W2114585931 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19128456" @default.
• W2114585931 hasPublicationYear "2009" @default.
• W2114585931 type Work @default.
• W2114585931 sameAs 2114585931 @default.
• W2114585931 citedByCount "71" @default.
• W2114585931 countsByYear W21145859312012 @default.
• W2114585931 countsByYear W21145859312013 @default.
• W2114585931 countsByYear W21145859312014 @default.
• W2114585931 countsByYear W21145859312015 @default.
• W2114585931 countsByYear W21145859312016 @default.
• W2114585931 countsByYear W21145859312017 @default.
• W2114585931 countsByYear W21145859312018 @default.
• W2114585931 countsByYear W21145859312019 @default.
• W2114585931 countsByYear W21145859312020 @default.
• W2114585931 countsByYear W21145859312021 @default.
• W2114585931 countsByYear W21145859312022 @default.
• W2114585931 countsByYear W21145859312023 @default.
• W2114585931 crossrefType "journal-article" @default.
• W2114585931 hasAuthorship W2114585931A5000153354 @default.
• W2114585931 hasAuthorship W2114585931A5004148079 @default.
• W2114585931 hasAuthorship W2114585931A5008407729 @default.
• W2114585931 hasAuthorship W2114585931A5051429563 @default.
• W2114585931 hasBestOaLocation W21145859311 @default.
• W2114585931 hasConcept C104317684 @default.
• W2114585931 hasConcept C111335760 @default.
• W2114585931 hasConcept C127561419 @default.
• W2114585931 hasConcept C143065580 @default.
• W2114585931 hasConcept C150194340 @default.
• W2114585931 hasConcept C153911025 @default.
• W2114585931 hasConcept C161733203 @default.
• W2114585931 hasConcept C184235292 @default.
• W2114585931 hasConcept C190283241 @default.
• W2114585931 hasConcept C502942594 @default.
• W2114585931 hasConcept C54009773 @default.
• W2114585931 hasConcept C54355233 @default.
• W2114585931 hasConcept C55493867 @default.
• W2114585931 hasConcept C81885089 @default.
• W2114585931 hasConcept C86803240 @default.
• W2114585931 hasConcept C95444343 @default.
• W2114585931 hasConceptScore W2114585931C104317684 @default.
• W2114585931 hasConceptScore W2114585931C111335760 @default.
• W2114585931 hasConceptScore W2114585931C127561419 @default.
• W2114585931 hasConceptScore W2114585931C143065580 @default.
• W2114585931 hasConceptScore W2114585931C150194340 @default.
• W2114585931 hasConceptScore W2114585931C153911025 @default.
• W2114585931 hasConceptScore W2114585931C161733203 @default.
• W2114585931 hasConceptScore W2114585931C184235292 @default.
• W2114585931 hasConceptScore W2114585931C190283241 @default.
• W2114585931 hasConceptScore W2114585931C502942594 @default.
• W2114585931 hasConceptScore W2114585931C54009773 @default.
• W2114585931 hasConceptScore W2114585931C54355233 @default.
• W2114585931 hasConceptScore W2114585931C55493867 @default.
• W2114585931 hasConceptScore W2114585931C81885089 @default.
• W2114585931 hasConceptScore W2114585931C86803240 @default.
• W2114585931 hasConceptScore W2114585931C95444343 @default.
• W2114585931 hasIssue "1" @default.
• W2114585931 hasLocation W21145859311 @default.
• W2114585931 hasLocation W21145859312 @default.
• W2114585931 hasLocation W21145859313 @default.
• W2114585931 hasLocation W21145859314 @default.
• W2114585931 hasOpenAccess W2114585931 @default.
• W2114585931 hasPrimaryLocation W21145859311 @default.
• W2114585931 hasRelatedWork W1692571807 @default.
• W2114585931 hasRelatedWork W1992273316 @default.
• W2114585931 hasRelatedWork W2063119860 @default.

• next