SLCO4A1-AS1 promotes colorectal tumourigenesis by regulating Cdk2/c-Myc signalling
Background SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumour...
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| Vydáno v: | Journal of biomedical science Ročník 29; číslo 1; s. 4 - 17 |
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| Hlavní autoři: | , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
BioMed Central
17.01.2022
BioMed Central Ltd Springer Nature B.V BMC |
| Témata: | |
| ISSN: | 1423-0127, 1021-7770, 1423-0127 |
| On-line přístup: | Získat plný text |
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| Abstract | Background
SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumourigenesis.
Methods
We measured the expression of SLCO4A1-AS1 in CRC tissues using qRT-PCR and determined its correlation with patient prognosis. Promoter methylation analyses were used to assess the methylation status of SLCO4A1-AS1. Gain- and loss-of-function assays were used to evaluate the effects of SLCO4A1-AS1 on CRC growth in vitro and in vivo. RNA pull-down, RNA immunoprecipitation, RNA-seq, luciferase reporter and immunohistochemistry assays were performed to identify the molecular mechanism of SLCO4A1-AS1 in CRC.
Results
SLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter. Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth.
Conclusions
Our data demonstrate that SLCO4A1-AS1 acts as an oncogene in CRC by regulating the Hsp90/Cdk2/c-Myc axis, supporting SLCO4A1-AS1 as a potential therapeutic target and prognostic factor for CRC. |
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| AbstractList | SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumourigenesis. We measured the expression of SLCO4A1-AS1 in CRC tissues using qRT-PCR and determined its correlation with patient prognosis. Promoter methylation analyses were used to assess the methylation status of SLCO4A1-AS1. Gain- and loss-of-function assays were used to evaluate the effects of SLCO4A1-AS1 on CRC growth in vitro and in vivo. RNA pull-down, RNA immunoprecipitation, RNA-seq, luciferase reporter and immunohistochemistry assays were performed to identify the molecular mechanism of SLCO4A1-AS1 in CRC. SLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter. Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth. Our data demonstrate that SLCO4A1-AS1 acts as an oncogene in CRC by regulating the Hsp90/Cdk2/c-Myc axis, supporting SLCO4A1-AS1 as a potential therapeutic target and prognostic factor for CRC. Abstract Background SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumourigenesis. Methods We measured the expression of SLCO4A1-AS1 in CRC tissues using qRT-PCR and determined its correlation with patient prognosis. Promoter methylation analyses were used to assess the methylation status of SLCO4A1-AS1. Gain- and loss-of-function assays were used to evaluate the effects of SLCO4A1-AS1 on CRC growth in vitro and in vivo. RNA pull-down, RNA immunoprecipitation, RNA-seq, luciferase reporter and immunohistochemistry assays were performed to identify the molecular mechanism of SLCO4A1-AS1 in CRC. Results SLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter. Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth. Conclusions Our data demonstrate that SLCO4A1-AS1 acts as an oncogene in CRC by regulating the Hsp90/Cdk2/c-Myc axis, supporting SLCO4A1-AS1 as a potential therapeutic target and prognostic factor for CRC. Background SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumourigenesis. Methods We measured the expression of SLCO4A1-AS1 in CRC tissues using qRT-PCR and determined its correlation with patient prognosis. Promoter methylation analyses were used to assess the methylation status of SLCO4A1-AS1. Gain- and loss-of-function assays were used to evaluate the effects of SLCO4A1-AS1 on CRC growth in vitro and in vivo. RNA pull-down, RNA immunoprecipitation, RNA-seq, luciferase reporter and immunohistochemistry assays were performed to identify the molecular mechanism of SLCO4A1-AS1 in CRC. Results SLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter. Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth. Conclusions Our data demonstrate that SLCO4A1-AS1 acts as an oncogene in CRC by regulating the Hsp90/Cdk2/c-Myc axis, supporting SLCO4A1-AS1 as a potential therapeutic target and prognostic factor for CRC. Keywords: Colorectal cancer, Long non-coding RNA, SLCO4A1-AS1, Cdk2, c-Myc SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumourigenesis. We measured the expression of SLCO4A1-AS1 in CRC tissues using qRT-PCR and determined its correlation with patient prognosis. Promoter methylation analyses were used to assess the methylation status of SLCO4A1-AS1. Gain- and loss-of-function assays were used to evaluate the effects of SLCO4A1-AS1 on CRC growth in vitro and in vivo. RNA pull-down, RNA immunoprecipitation, RNA-seq, luciferase reporter and immunohistochemistry assays were performed to identify the molecular mechanism of SLCO4A1-AS1 in CRC. SLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter. Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth. Our data demonstrate that SLCO4A1-AS1 acts as an oncogene in CRC by regulating the Hsp90/Cdk2/c-Myc axis, supporting SLCO4A1-AS1 as a potential therapeutic target and prognostic factor for CRC. Background SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumourigenesis. Methods We measured the expression of SLCO4A1-AS1 in CRC tissues using qRT-PCR and determined its correlation with patient prognosis. Promoter methylation analyses were used to assess the methylation status of SLCO4A1-AS1. Gain- and loss-of-function assays were used to evaluate the effects of SLCO4A1-AS1 on CRC growth in vitro and in vivo. RNA pull-down, RNA immunoprecipitation, RNA-seq, luciferase reporter and immunohistochemistry assays were performed to identify the molecular mechanism of SLCO4A1-AS1 in CRC. Results SLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter. Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth. Conclusions Our data demonstrate that SLCO4A1-AS1 acts as an oncogene in CRC by regulating the Hsp90/Cdk2/c-Myc axis, supporting SLCO4A1-AS1 as a potential therapeutic target and prognostic factor for CRC. SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumourigenesis.BACKGROUNDSLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumourigenesis.We measured the expression of SLCO4A1-AS1 in CRC tissues using qRT-PCR and determined its correlation with patient prognosis. Promoter methylation analyses were used to assess the methylation status of SLCO4A1-AS1. Gain- and loss-of-function assays were used to evaluate the effects of SLCO4A1-AS1 on CRC growth in vitro and in vivo. RNA pull-down, RNA immunoprecipitation, RNA-seq, luciferase reporter and immunohistochemistry assays were performed to identify the molecular mechanism of SLCO4A1-AS1 in CRC.METHODSWe measured the expression of SLCO4A1-AS1 in CRC tissues using qRT-PCR and determined its correlation with patient prognosis. Promoter methylation analyses were used to assess the methylation status of SLCO4A1-AS1. Gain- and loss-of-function assays were used to evaluate the effects of SLCO4A1-AS1 on CRC growth in vitro and in vivo. RNA pull-down, RNA immunoprecipitation, RNA-seq, luciferase reporter and immunohistochemistry assays were performed to identify the molecular mechanism of SLCO4A1-AS1 in CRC.SLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter. Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth.RESULTSSLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter. Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth.Our data demonstrate that SLCO4A1-AS1 acts as an oncogene in CRC by regulating the Hsp90/Cdk2/c-Myc axis, supporting SLCO4A1-AS1 as a potential therapeutic target and prognostic factor for CRC.CONCLUSIONSOur data demonstrate that SLCO4A1-AS1 acts as an oncogene in CRC by regulating the Hsp90/Cdk2/c-Myc axis, supporting SLCO4A1-AS1 as a potential therapeutic target and prognostic factor for CRC. Background SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to be elucidated. Therefore, we investigated the functions, mechanism, and clinical significance of SLCO4A1-AS1 in colorectal tumourigenesis. Methods We measured the expression of SLCO4A1-AS1 in CRC tissues using qRT-PCR and determined its correlation with patient prognosis. Promoter methylation analyses were used to assess the methylation status of SLCO4A1-AS1. Gain- and loss-of-function assays were used to evaluate the effects of SLCO4A1-AS1 on CRC growth in vitro and in vivo. RNA pull-down, RNA immunoprecipitation, RNA-seq, luciferase reporter and immunohistochemistry assays were performed to identify the molecular mechanism of SLCO4A1-AS1 in CRC. Results SLCO4A1-AS1 was frequently upregulated in CRC tissues based on multiple CRC cohorts and was associated with poor prognoses. Aberrant overexpression of SLCO4A1-AS1 in CRC is partly attributed to the DNA hypomethylation of its promoter. Ectopic SLCO4A1-AS1 expression promoted CRC cell growth, whereas SLCO4A1-AS1 knockdown repressed CRC proliferation both in vitro and in vivo. Mechanistic investigations revealed that SLCO4A1-AS1 functions as a molecular scaffold to strengthen the interaction between Hsp90 and Cdk2, promoting the protein stability of Cdk2. The SLCO4A1-AS1-induced increase in Cdk2 levels activates the c-Myc signalling pathway by promoting the phosphorylation of c-Myc at Ser62, resulting in increased tumour growth. Conclusions Our data demonstrate that SLCO4A1-AS1 acts as an oncogene in CRC by regulating the Hsp90/Cdk2/c-Myc axis, supporting SLCO4A1-AS1 as a potential therapeutic target and prognostic factor for CRC. |
| ArticleNumber | 4 |
| Audience | Academic |
| Author | Cui, Kaisa Zhou, Leyuan Fei, Bojian Yin, Yuan Wang, Xue Huang, Shengling Bian, Zehua Yang, Fan Li, Chaoqun Huang, Liuying Sun, Shengbai Zhang, Jia Huang, Zhaohui |
| Author_xml | – sequence: 1 givenname: Jia surname: Zhang fullname: Zhang, Jia organization: Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University – sequence: 2 givenname: Kaisa surname: Cui fullname: Cui, Kaisa organization: Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University – sequence: 3 givenname: Liuying surname: Huang fullname: Huang, Liuying organization: Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University – sequence: 4 givenname: Fan surname: Yang fullname: Yang, Fan organization: Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University – sequence: 5 givenname: Shengbai surname: Sun fullname: Sun, Shengbai organization: Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University – sequence: 6 givenname: Zehua surname: Bian fullname: Bian, Zehua organization: Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University – sequence: 7 givenname: Xue surname: Wang fullname: Wang, Xue organization: Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University – sequence: 8 givenname: Chaoqun surname: Li fullname: Li, Chaoqun organization: Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University – sequence: 9 givenname: Yuan surname: Yin fullname: Yin, Yuan organization: Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University – sequence: 10 givenname: Shengling surname: Huang fullname: Huang, Shengling organization: Institutes of Biomedical Sciences and Shanghai Cancer Center, Shanghai Medical College, Fudan University – sequence: 11 givenname: Leyuan surname: Zhou fullname: Zhou, Leyuan organization: Department of Radiation Oncology, Affiliated Hospital of Jiangnan University – sequence: 12 givenname: Bojian surname: Fei fullname: Fei, Bojian organization: Department of Surgical Oncology, Affiliated Hospital of Jiangnan University – sequence: 13 givenname: Zhaohui surname: Huang fullname: Huang, Zhaohui email: zhaohuihuang@jiangnan.edu.cn organization: Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Laboratory of Cancer Epigenetics, Wuxi School of Medicine, Jiangnan University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35039060$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1073/pnas.0900121106 10.4161/cc.7.18.6701 10.1038/s41392-020-00446-7 10.1186/s13046-018-0896-y 10.1111/odi.13893 10.1016/j.drudis.2019.12.001 10.1002/ijc.29226 10.1021/bi051423m 10.1101/gad.836800 10.7150/ijbs.38041 10.1016/j.molcel.2007.01.001 10.1073/pnas.0506580102 10.1038/cr.2014.35 10.1002/cam4.3270 10.2147/OTT.S191740 10.3389/fonc.2019.01269 10.1016/j.prp.2020.153104 10.1016/j.ebiom.2021.103399 10.1002/cam4.3830 10.18632/aging.102081 10.2217/epi.09.33 10.1016/j.ebiom.2018.03.032 10.1002/hep.29405 10.1038/srep23892 10.1002/cam4.2105 10.1089/omi.2011.0118 10.1056/NEJM200007133430201 10.1186/s13046-020-01783-9 10.1007/978-1-4939-2425-7_25 10.1080/15384047.2020.1787757 10.1158/1078-0432.CCR-17-2967 10.1038/nrm.2017.20 10.1186/1476-4598-11-5 10.1038/s41374-021-00577-7 10.1111/ijlh.13501 10.1016/j.cell.2012.03.003 10.1038/s41389-017-0008-4 10.1038/s41392-021-00624-1 |
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| DOI | 10.1186/s12929-022-00789-z |
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| References | Y Liu (789_CR28) 2007; 25 B Liu (789_CR13) 2020; 216 K Augoff (789_CR3) 2012; 11 Z Yang (789_CR36) 2021; 68 789_CR23 Z Huang (789_CR22) 2015; 136 J Mao (789_CR37) 2021; 43 P Hydbring (789_CR31) 2010; 107 I Pashtan (789_CR39) 2008; 7 Y Yang (789_CR33) 2019; 12 JF Xiang (789_CR4) 2014; 24 K Wu (789_CR17) 2021; 101 Y Wei (789_CR16) 2020; 9 J Zhang (789_CR34) 2018; 67 H Sung (789_CR1) 2021; 71 T Yan (789_CR7) 2021; 6 T Prince (789_CR30) 2005; 44 F Zhang (789_CR35) 2021 Z Wang (789_CR19) 2019; 11 Z Bian (789_CR10) 2016; 6 Z Bian (789_CR11) 2017; 6 J Yu (789_CR21) 2018; 37 FH Schopf (789_CR27) 2017; 18 M Zhou (789_CR12) 2021; 10 Z Bian (789_CR9) 2018; 24 Q Li (789_CR18) 2020; 21 A Subramanian (789_CR24) 2005; 102 M Ehrlich (789_CR26) 2009; 1 Y Zhu (789_CR6) 2018; 30 Y Liu (789_CR15) 2019; 9 RC Sears (789_CR32) 2000; 14 S Tadesse (789_CR38) 2020; 25 X Hu (789_CR8) 2020; 39 P Lichtenstein (789_CR2) 2000; 343 L Cai (789_CR29) 2021; 6 V Dang Chi (789_CR40) 2012; 149 R Tang (789_CR20) 2019; 15 SK Qingyu (789_CR5) 2016; 2 M Li (789_CR14) 2019; 8 G Yu (789_CR25) 2012; 16 |
| References_xml | – volume: 107 start-page: 58 issue: 1 year: 2010 ident: 789_CR31 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0900121106 – volume: 7 start-page: 2936 issue: 18 year: 2008 ident: 789_CR39 publication-title: Cell Cycle doi: 10.4161/cc.7.18.6701 – volume: 6 start-page: 70 issue: 1 year: 2021 ident: 789_CR7 publication-title: Signal Transduct Target Ther doi: 10.1038/s41392-020-00446-7 – volume: 37 start-page: 222 issue: 1 year: 2018 ident: 789_CR21 publication-title: J Exp Clin Cancer Res doi: 10.1186/s13046-018-0896-y – year: 2021 ident: 789_CR35 publication-title: Oral Dis. doi: 10.1111/odi.13893 – volume: 25 start-page: 406 issue: 2 year: 2020 ident: 789_CR38 publication-title: Drug Discov Today doi: 10.1016/j.drudis.2019.12.001 – volume: 136 start-page: 1792 issue: 8 year: 2015 ident: 789_CR22 publication-title: Int J Cancer doi: 10.1002/ijc.29226 – volume: 44 start-page: 15287 issue: 46 year: 2005 ident: 789_CR30 publication-title: Biochemistry doi: 10.1021/bi051423m – volume: 14 start-page: 2501 issue: 19 year: 2000 ident: 789_CR32 publication-title: Genes Dev doi: 10.1101/gad.836800 – volume: 2 start-page: 11 issue: 2 year: 2016 ident: 789_CR5 publication-title: Biomed Sci. – volume: 15 start-page: 2885 issue: 13 year: 2019 ident: 789_CR20 publication-title: Int J Biol Sci doi: 10.7150/ijbs.38041 – volume: 25 start-page: 207 issue: 2 year: 2007 ident: 789_CR28 publication-title: Mol Cell doi: 10.1016/j.molcel.2007.01.001 – volume: 102 start-page: 15545 issue: 43 year: 2005 ident: 789_CR24 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0506580102 – volume: 24 start-page: 513 issue: 5 year: 2014 ident: 789_CR4 publication-title: Cell Res doi: 10.1038/cr.2014.35 – volume: 9 start-page: 7205 issue: 19 year: 2020 ident: 789_CR16 publication-title: Cancer Med. doi: 10.1002/cam4.3270 – volume: 12 start-page: 1351 year: 2019 ident: 789_CR33 publication-title: Onco Targets Ther doi: 10.2147/OTT.S191740 – volume: 9 start-page: 1269 year: 2019 ident: 789_CR15 publication-title: Front Oncol doi: 10.3389/fonc.2019.01269 – volume: 216 start-page: 153104 issue: 10 year: 2020 ident: 789_CR13 publication-title: Pathol Res Pract. doi: 10.1016/j.prp.2020.153104 – volume: 68 start-page: 103399 year: 2021 ident: 789_CR36 publication-title: EBioMedicine. doi: 10.1016/j.ebiom.2021.103399 – volume: 10 start-page: 2470 issue: 7 year: 2021 ident: 789_CR12 publication-title: Cancer Med. doi: 10.1002/cam4.3830 – volume: 11 start-page: 4876 issue: 14 year: 2019 ident: 789_CR19 publication-title: Aging (Albany NY) doi: 10.18632/aging.102081 – volume: 1 start-page: 239 year: 2009 ident: 789_CR26 publication-title: Epigenomics doi: 10.2217/epi.09.33 – volume: 71 start-page: 209 issue: 3 year: 2021 ident: 789_CR1 publication-title: CA. – volume: 30 start-page: 148 year: 2018 ident: 789_CR6 publication-title: EBioMedicine doi: 10.1016/j.ebiom.2018.03.032 – volume: 67 start-page: 171 issue: 1 year: 2018 ident: 789_CR34 publication-title: Hepatology doi: 10.1002/hep.29405 – volume: 6 start-page: 23892 year: 2016 ident: 789_CR10 publication-title: Sci Rep doi: 10.1038/srep23892 – volume: 8 start-page: 2404 issue: 5 year: 2019 ident: 789_CR14 publication-title: Cancer Med doi: 10.1002/cam4.2105 – volume: 16 start-page: 284 issue: 5 year: 2012 ident: 789_CR25 publication-title: OMICS doi: 10.1089/omi.2011.0118 – volume: 343 start-page: 78 issue: 2 year: 2000 ident: 789_CR2 publication-title: N Engl J Med doi: 10.1056/NEJM200007133430201 – volume: 39 start-page: 270 issue: 1 year: 2020 ident: 789_CR8 publication-title: J Exp Clin Cancer Res doi: 10.1186/s13046-020-01783-9 – ident: 789_CR23 doi: 10.1007/978-1-4939-2425-7_25 – volume: 21 start-page: 806 issue: 9 year: 2020 ident: 789_CR18 publication-title: Cancer Biol Ther doi: 10.1080/15384047.2020.1787757 – volume: 24 start-page: 4808 issue: 19 year: 2018 ident: 789_CR9 publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-17-2967 – volume: 18 start-page: 345 issue: 6 year: 2017 ident: 789_CR27 publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm.2017.20 – volume: 11 start-page: 5 year: 2012 ident: 789_CR3 publication-title: Mol Cancer doi: 10.1186/1476-4598-11-5 – volume: 101 start-page: 908 issue: 7 year: 2021 ident: 789_CR17 publication-title: Lab Invest. doi: 10.1038/s41374-021-00577-7 – volume: 43 start-page: 1050 issue: 5 year: 2021 ident: 789_CR37 publication-title: Int J Lab Hematol. doi: 10.1111/ijlh.13501 – volume: 149 start-page: 22 issue: 1 year: 2012 ident: 789_CR40 publication-title: Cell doi: 10.1016/j.cell.2012.03.003 – volume: 6 start-page: 1 issue: 11 year: 2017 ident: 789_CR11 publication-title: Oncogenesis doi: 10.1038/s41389-017-0008-4 – volume: 6 start-page: 276 issue: 1 year: 2021 ident: 789_CR29 publication-title: Signal Transduct Target Ther doi: 10.1038/s41392-021-00624-1 |
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SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in... SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in CRC remain to... Background SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of SLCO4A1-AS1 in... Abstract Background SLCO4A1-AS1 was found to be upregulated in several cancer types, including colorectal cancer (CRC). However, the detailed roles of... |
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| SubjectTerms | Analysis Antibodies Biomedical and Life Sciences Biomedicine c-Myc c-Myc protein Cancer Carcinogenesis - genetics Cdk2 Cell cycle Cell growth Cell Line, Tumor Cell Movement Cell Proliferation - genetics Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Cyclin-Dependent Kinase 2 DNA methylation Gene Expression Regulation, Neoplastic Genes Heat shock proteins Hsp90 protein Humans Immunohistochemistry Immunoprecipitation In vivo methods and tests Long non-coding RNA Mass spectrometry Metastasis Methylation MicroRNAs Myc protein Pathogenesis Phosphorylation Plasmids Prognosis Proteins Proto-Oncogene Proteins c-myc Ribonucleic acid RNA RNA, Antisense RNA, Long Noncoding Scientific imaging Signal transduction Signal Transduction - genetics Signaling SLCO4A1-AS1 Therapeutic targets Tumorigenesis Tumors |
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| Title | SLCO4A1-AS1 promotes colorectal tumourigenesis by regulating Cdk2/c-Myc signalling |
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