FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2804412686> ?p ?o ?g. }

• W2804412686 abstract "Dysregulation of transforming growth factor β (TGF-β) signaling and hypoxic microenvironment have respectively been reported to be involved in disease progression in malignancies of prostate. Emerging evidence indicates that downregulation of TGFBR2, a pivotal regulator of TGF-β signaling, may contribute to carcinogenesis and progression of prostate cancer (PCa). However, the biological function and regulatory mechanism of TGFBR2 in PCa remain poorly understood. In this study, we propose to investigate the crosstalk of hypoxia and TGF-β signaling and provide insight into the molecular mechanism underlying the regulatory pathways in PCa. Prostate cancer cell lines were cultured in hypoxia or normoxia to evaluate the effect of hypoxia on TGFBR2 expression. Methylation specific polymerase chain reaction (MSP) and demethylation agents was used to evaluate the methylation regulation of TGFBR2 promoter. Besides, silencing of EZH2 via specific siRNAs or chemical inhibitor was used to validate the regulatory effect of EZH2 on TGFBR2. Moreover, we conducted PCR, western blot, and luciferase assays which studied the relationship of miR-93 and TGFBR2 in PCa cell lines and specimens. We also detected the impacts of hypoxia on EZH2 and miR-93, and further examined the tumorigenic functions of miR-93 on proliferation and epithelial-mesenchymal transition via a series of experiments. TGFBR2 expression was attenuated under hypoxia. Hypoxia-induced EZH2 promoted H3K27me3 which caused TGFBR2 promoter hypermethylation and contributed to its epigenetic silencing in PCa. Besides, miR-93 was significantly upregulated in PCa tissues and cell lines, and negatively correlated with the expression of TGFBR2. Ectopic expression of miR-93 promoted cell proliferation, migration and invasion in PCa, and its expression could also be induced by hypoxia. In addition, TGFBR2 was identified as a bona fide target of miR-93. Our findings elucidate diverse hypoxia-regulated pathways including EZH2-mediated hypermethylation and miR-93-induced silencing contribute to attenuation of TGFBR2 expression and promote cancer progression in prostate cancer." @default.
• W2804412686 created "2018-06-01" @default.
• W2804412686 creator A5005098292 @default.
• W2804412686 creator A5006157075 @default.
• W2804412686 creator A5008716861 @default.
• W2804412686 creator A5009338281 @default.
• W2804412686 creator A5011480176 @default.
• W2804412686 creator A5020117680 @default.
• W2804412686 creator A5026000971 @default.
• W2804412686 creator A5042012998 @default.
• W2804412686 creator A5059068739 @default.
• W2804412686 creator A5079886307 @default.
• W2804412686 creator A5080492467 @default.
• W2804412686 date "2018-04-27" @default.
• W2804412686 modified "2023-10-17" @default.
• W2804412686 title "Attenuation of TGFBR2 expression and tumour progression in prostate cancer involve diverse hypoxia-regulated pathways" @default.
• W2804412686 cites W1159619803 @default.
• W2804412686 cites W1493048246 @default.
• W2804412686 cites W1930757702 @default.
• W2804412686 cites W1976897524 @default.
• W2804412686 cites W1978660434 @default.
• W2804412686 cites W1989829282 @default.
• W2804412686 cites W1992761930 @default.
• W2804412686 cites W2002702229 @default.
• W2804412686 cites W2003496908 @default.
• W2804412686 cites W2026335777 @default.
• W2804412686 cites W2029197798 @default.
• W2804412686 cites W2033178140 @default.
• W2804412686 cites W2034622310 @default.
• W2804412686 cites W2040182688 @default.
• W2804412686 cites W2040452711 @default.
• W2804412686 cites W2083365530 @default.
• W2804412686 cites W2104825362 @default.
• W2804412686 cites W2105998513 @default.
• W2804412686 cites W2108337681 @default.
• W2804412686 cites W2117460748 @default.
• W2804412686 cites W2118655588 @default.
• W2804412686 cites W2132758869 @default.
• W2804412686 cites W2139405623 @default.
• W2804412686 cites W2150095882 @default.
• W2804412686 cites W2153784080 @default.
• W2804412686 cites W2155979487 @default.
• W2804412686 cites W2164012646 @default.
• W2804412686 cites W2165241843 @default.
• W2804412686 cites W2251776775 @default.
• W2804412686 cites W2264436887 @default.
• W2804412686 cites W2332099868 @default.
• W2804412686 cites W2374829764 @default.
• W2804412686 cites W2418050294 @default.
• W2804412686 cites W2517261003 @default.
• W2804412686 cites W2561840259 @default.
• W2804412686 cites W2570618306 @default.
• W2804412686 cites W2727380696 @default.
• W2804412686 cites W2737325271 @default.
• W2804412686 cites W2755550738 @default.
• W2804412686 cites W7383260 @default.
• W2804412686 doi "https://doi.org/10.1186/s13046-018-0764-9" @default.
• W2804412686 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5921809" @default.
• W2804412686 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29699590" @default.
• W2804412686 hasPublicationYear "2018" @default.
• W2804412686 type Work @default.
• W2804412686 sameAs 2804412686 @default.
• W2804412686 citedByCount "28" @default.
• W2804412686 countsByYear W28044126862018 @default.
• W2804412686 countsByYear W28044126862019 @default.
• W2804412686 countsByYear W28044126862020 @default.
• W2804412686 countsByYear W28044126862021 @default.
• W2804412686 countsByYear W28044126862022 @default.
• W2804412686 countsByYear W28044126862023 @default.
• W2804412686 crossrefType "journal-article" @default.
• W2804412686 hasAuthorship W2804412686A5005098292 @default.
• W2804412686 hasAuthorship W2804412686A5006157075 @default.
• W2804412686 hasAuthorship W2804412686A5008716861 @default.
• W2804412686 hasAuthorship W2804412686A5009338281 @default.
• W2804412686 hasAuthorship W2804412686A5011480176 @default.
• W2804412686 hasAuthorship W2804412686A5020117680 @default.
• W2804412686 hasAuthorship W2804412686A5026000971 @default.
• W2804412686 hasAuthorship W2804412686A5042012998 @default.
• W2804412686 hasAuthorship W2804412686A5059068739 @default.
• W2804412686 hasAuthorship W2804412686A5079886307 @default.
• W2804412686 hasAuthorship W2804412686A5080492467 @default.
• W2804412686 hasBestOaLocation W28044126861 @default.
• W2804412686 hasConcept C104317684 @default.
• W2804412686 hasConcept C119056186 @default.
• W2804412686 hasConcept C121608353 @default.
• W2804412686 hasConcept C127561419 @default.
• W2804412686 hasConcept C150194340 @default.
• W2804412686 hasConcept C185592680 @default.
• W2804412686 hasConcept C190727270 @default.
• W2804412686 hasConcept C2780192828 @default.
• W2804412686 hasConcept C41091548 @default.
• W2804412686 hasConcept C50171091 @default.
• W2804412686 hasConcept C502942594 @default.
• W2804412686 hasConcept C54355233 @default.
• W2804412686 hasConcept C55493867 @default.
• W2804412686 hasConcept C555283112 @default.
• W2804412686 hasConcept C62112901 @default.
• W2804412686 hasConcept C62478195 @default.
• W2804412686 hasConcept C76419328 @default.
• W2804412686 hasConcept C86803240 @default.

• next