FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2167226090> ?p ?o ?g. }

• W2167226090 endingPage "2035" @default.
• W2167226090 startingPage "2025" @default.
• W2167226090 abstract "As an important epigenetic mechanism, histone acetylation modulates the transcription of many genes and plays important roles in hepatocellular carcinoma (HCC). Aberrations in histone acetylation have been observed in HCC, but the factors that contribute to the aberrations have not been fully elucidated. MicroRNAs (miRNAs), which are noncoding RNAs that regulate gene expression, are involved in important epigenetic mechanisms. In this study, we determined that miR-200a and the level of histone H3 acetylation at its promoter were reduced in human HCC tissues in comparison with adjacent noncancerous hepatic tissues. Furthermore, our results suggested that the histone deacetylase 4 (HDAC4) inhibited the expression of miR-200a and its promoter activity and reduced the histone H3 acetylation level at the mir-200a promoter through a Sp1-dependent pathway. Interestingly, we observed that the miR-200a directly targeted the 3′-untranslated region of the HDAC4 messenger RNA and repressed expression of HDAC4. Therefore, miR-200a ultimately induced its own transcription and increased the histone H3 acetylation level at its own promoter. Through targeting HDAC4, miR-200a also induced the up-regulation of total acetyl-histone H3 levels and increased the histone H3 acetylation level at the p21WAF/Cip1 promoter. Finally, we determined that miR-200a inhibited the proliferation and migration of HCC cells in vivo and in vitro. Conclusion: Our findings suggest that the HDAC4/Sp1/miR-200a regulatory network induces the down-regulation of miR-200a and the up-regulation of HDAC4 in HCC. As a result, down-regulation of miR-200a enhances the proliferation and migration of HCC cells and induces aberrant histone acetylation in HCC. These findings highlight a potential therapeutic approach in targeting the HDAC4/Sp1/miR-200a regulatory network for the treatment of HCC. (HEPATOLOGY 2011" @default.
• W2167226090 created "2016-06-24" @default.
• W2167226090 creator A5002661071 @default.
• W2167226090 creator A5011231204 @default.
• W2167226090 creator A5031246881 @default.
• W2167226090 creator A5033299593 @default.
• W2167226090 creator A5041557804 @default.
• W2167226090 creator A5041799538 @default.
• W2167226090 creator A5067013860 @default.
• W2167226090 creator A5081157403 @default.
• W2167226090 date "2011-12-01" @default.
• W2167226090 modified "2023-09-28" @default.
• W2167226090 title "The histone deacetylase 4/SP1/microrna-200a regulatory network contributes to aberrant histone acetylation in hepatocellular carcinoma" @default.
• W2167226090 cites W144423133 @default.
• W2167226090 cites W1965448600 @default.
• W2167226090 cites W1974692834 @default.
• W2167226090 cites W1975514993 @default.
• W2167226090 cites W1976324983 @default.
• W2167226090 cites W1976888700 @default.
• W2167226090 cites W1986903527 @default.
• W2167226090 cites W1999260149 @default.
• W2167226090 cites W2001502548 @default.
• W2167226090 cites W2010093803 @default.
• W2167226090 cites W2017270642 @default.
• W2167226090 cites W2022165152 @default.
• W2167226090 cites W2023386504 @default.
• W2167226090 cites W2029148944 @default.
• W2167226090 cites W2036169252 @default.
• W2167226090 cites W2048280970 @default.
• W2167226090 cites W2050869737 @default.
• W2167226090 cites W2052041317 @default.
• W2167226090 cites W2052373759 @default.
• W2167226090 cites W2056768380 @default.
• W2167226090 cites W2057846741 @default.
• W2167226090 cites W2061743943 @default.
• W2167226090 cites W2075198755 @default.
• W2167226090 cites W2092035608 @default.
• W2167226090 cites W2093593077 @default.
• W2167226090 cites W2099008463 @default.
• W2167226090 cites W2099780774 @default.
• W2167226090 cites W2103177465 @default.
• W2167226090 cites W2107462637 @default.
• W2167226090 cites W2108017291 @default.
• W2167226090 cites W2109261002 @default.
• W2167226090 cites W2112666597 @default.
• W2167226090 cites W2117391818 @default.
• W2167226090 cites W2137052325 @default.
• W2167226090 cites W2148104254 @default.
• W2167226090 cites W2158747282 @default.
• W2167226090 cites W2168368163 @default.
• W2167226090 cites W3190412754 @default.
• W2167226090 doi "https://doi.org/10.1002/hep.24606" @default.
• W2167226090 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21837748" @default.
• W2167226090 hasPublicationYear "2011" @default.
• W2167226090 type Work @default.
• W2167226090 sameAs 2167226090 @default.
• W2167226090 citedByCount "155" @default.
• W2167226090 countsByYear W21672260902012 @default.
• W2167226090 countsByYear W21672260902013 @default.
• W2167226090 countsByYear W21672260902014 @default.
• W2167226090 countsByYear W21672260902015 @default.
• W2167226090 countsByYear W21672260902016 @default.
• W2167226090 countsByYear W21672260902017 @default.
• W2167226090 countsByYear W21672260902018 @default.
• W2167226090 countsByYear W21672260902019 @default.
• W2167226090 countsByYear W21672260902020 @default.
• W2167226090 countsByYear W21672260902021 @default.
• W2167226090 countsByYear W21672260902022 @default.
• W2167226090 countsByYear W21672260902023 @default.
• W2167226090 crossrefType "journal-article" @default.
• W2167226090 hasAuthorship W2167226090A5002661071 @default.
• W2167226090 hasAuthorship W2167226090A5011231204 @default.
• W2167226090 hasAuthorship W2167226090A5031246881 @default.
• W2167226090 hasAuthorship W2167226090A5033299593 @default.
• W2167226090 hasAuthorship W2167226090A5041557804 @default.
• W2167226090 hasAuthorship W2167226090A5041799538 @default.
• W2167226090 hasAuthorship W2167226090A5067013860 @default.
• W2167226090 hasAuthorship W2167226090A5081157403 @default.
• W2167226090 hasBestOaLocation W21672260901 @default.
• W2167226090 hasConcept C104317684 @default.
• W2167226090 hasConcept C119157956 @default.
• W2167226090 hasConcept C145059251 @default.
• W2167226090 hasConcept C153911025 @default.
• W2167226090 hasConcept C27253355 @default.
• W2167226090 hasConcept C2776745794 @default.
• W2167226090 hasConcept C2778305200 @default.
• W2167226090 hasConcept C41091548 @default.
• W2167226090 hasConcept C45946802 @default.
• W2167226090 hasConcept C4951695 @default.
• W2167226090 hasConcept C502942594 @default.
• W2167226090 hasConcept C55493867 @default.
• W2167226090 hasConcept C58793620 @default.
• W2167226090 hasConcept C64927066 @default.
• W2167226090 hasConcept C71723506 @default.
• W2167226090 hasConcept C86803240 @default.
• W2167226090 hasConcept C95444343 @default.
• W2167226090 hasConceptScore W2167226090C104317684 @default.
• W2167226090 hasConceptScore W2167226090C119157956 @default.

• next