
DOI . ORG {
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Title[redir]:
Increased expression of long noncoding RNA TUG1 predicts a poor prognosis of gastric cancer and regulates cell proliferation by epigenetically silencing of p57 | Cell Death & Disease
Description:
Recent evidence highlights long noncoding RNAs (lncRNAs) as crucial regulators of cancer biology that contribute to tumorigenesis. LncRNA TUG1 was initially detected in a genomic screen for genes upregulated in response to taurine treatment in developing mouse retinal cells. Our previous study showed that TUG1 could affect cell proliferation through epigenetically regulating HOXB7 in human non-small cell lung cancer. However, the clinical significance and potential role of TUG1 in GC remains unclear. In this study, we found that TUG1 is significantly increased and is correlated with outcomes in gastric cancer (GC). Further experiments revealed that knockdown of TUG1 repressed GC proliferation both in vitro and in vivo. Mechanistic investigations showed that TUG1 has a key role in G0/G1 arrest. We further demonstrated that TUG1 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15, p16, p21, p27 and p57, thus contributing to the regulation of GC cell cycle and proliferation. Together, our results suggest that TUG1, as a regulator of proliferation, may serve as a candidate prognostic biomarker and target for new therapies in human GC.
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Keywords {๐}
tug, cell, expression, article, cells, cancer, google, scholar, cas, rna, proliferation, noncoding, figure, ezh, tissues, long, results, analysis, tumor, gastric, showed, cycle, prc, nature, study, ags, role, knockdown, zhang, lncrnas, gene, transfected, yin, human, protein, patients, qrtpcr, upregulated, progression, survival, development, ckis, performed, assays, usa, rnas, found, regulation, level, bgc,
Topics {โ๏ธ}
open-access journal published nature publishing group nature portfolio privacy policy translational cancer research previous research showed research ethics committee advertising si-nc/si-tug1/si-tug1+vector previous research suggested nature 2009 nature 2010 nature specific pathogen-free conditions anti-suz12 rna-ip fraction 0/ reprints g1โg0 phase arrest mir-99a/mir-449a g1โg0 phase compared limited protein-coding potential tissue-specific expression pattern genome-wide rna immunoprecipitation activation-induced cytidine deaminase quantitative real-time pcr regulates cell proliferation social media long noncoding rna long noncoding rnas real-time pcr analyses log-rank test applied shctrl/shtug1-transfected ags cells g0/g1 arrest permissions si-nc/si-ezh2 tug1-mediated proliferation regulation noncoding rna malat1 sponging mir-331-3p media promotes cell proliferation chromatin signature reveals kaplanโmeier survival analysis cell signaling technology cell death dis embryonic ectoderm development mouse retinal development g1 phase compared prc2-mediated epigenetic regulation block retinal development methods tissue collection coding rna anril
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headline:Increased expression of long noncoding RNA TUG1 predicts a poor prognosis of gastric cancer and regulates cell proliferation by epigenetically silencing of p57
description:Recent evidence highlights long noncoding RNAs (lncRNAs) as crucial regulators of cancer biology that contribute to tumorigenesis. LncRNA TUG1 was initially detected in a genomic screen for genes upregulated in response to taurine treatment in developing mouse retinal cells. Our previous study showed that TUG1 could affect cell proliferation through epigenetically regulating HOXB7 in human non-small cell lung cancer. However, the clinical significance and potential role of TUG1 in GC remains unclear. In this study, we found that TUG1 is significantly increased and is correlated with outcomes in gastric cancer (GC). Further experiments revealed that knockdown of TUG1 repressed GC proliferation both in vitro and in vivo. Mechanistic investigations showed that TUG1 has a key role in G0/G1 arrest. We further demonstrated that TUG1 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15, p16, p21, p27 and p57, thus contributing to the regulation of GC cell cycle and proliferation. Together, our results suggest that TUG1, as a regulator of proliferation, may serve as a candidate prognostic biomarker and target for new therapies in human GC.
datePublished:2016-02-25T00:00:00Z
dateModified:2016-02-25T00:00:00Z
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Gastric cancer
Gene silencing
Non-coding RNAs
Prognostic markers
Life Sciences
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Biochemistry
Cell Biology
Immunology
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Antibodies
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headline:Increased expression of long noncoding RNA TUG1 predicts a poor prognosis of gastric cancer and regulates cell proliferation by epigenetically silencing of p57
description:Recent evidence highlights long noncoding RNAs (lncRNAs) as crucial regulators of cancer biology that contribute to tumorigenesis. LncRNA TUG1 was initially detected in a genomic screen for genes upregulated in response to taurine treatment in developing mouse retinal cells. Our previous study showed that TUG1 could affect cell proliferation through epigenetically regulating HOXB7 in human non-small cell lung cancer. However, the clinical significance and potential role of TUG1 in GC remains unclear. In this study, we found that TUG1 is significantly increased and is correlated with outcomes in gastric cancer (GC). Further experiments revealed that knockdown of TUG1 repressed GC proliferation both in vitro and in vivo. Mechanistic investigations showed that TUG1 has a key role in G0/G1 arrest. We further demonstrated that TUG1 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors, including p15, p16, p21, p27 and p57, thus contributing to the regulation of GC cell cycle and proliferation. Together, our results suggest that TUG1, as a regulator of proliferation, may serve as a candidate prognostic biomarker and target for new therapies in human GC.
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Gene silencing
Non-coding RNAs
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Antibodies
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