MicroRNA-139 inhibits hepatocellular carcinoma cell growth through down-regulating karyopherin alpha 2

MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC remains largely unknown. We investigated the function in human cell lines and patient tissue samples by experimental techniques in molecular...

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Published inJournal of experimental & clinical cancer research Vol. 38; no. 1; pp. 182 - 15
Main Authors Zan, Ying, Wang, Baofeng, Liang, Liang, Deng, Yujiao, Tian, Tian, Dai, Zhijun, Dong, Lei
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 02.05.2019
BioMed Central
BMC
Subjects
Analysis
Apoptosis
Binding sites
Biomarkers
Breast cancer
Cancer
Cancer therapies
Carcinoma
Care and treatment
Cell cycle
Cell growth
Cells (Biology)
Colony formation
Colorectal cancer
Development and progression
Epithelial-to-mesenchymal transition
Gastric cancer
Gene expression
Genetic aspects
Growth
Hepatocellular carcinoma
Kinases
Liver cancer
Medical prognosis
Metastasis
MicroRNA
MicroRNAs
Migration and invasion
Molecular biology
Patients
Phenotypes
Physiological aspects
Proteins
Roles
Statistics
Stem cells
Studies
Surgery
Survival
China
United States > US
Migration and invasion
Colony formation
Survival
Epithelial-to-mesenchymal transition
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Abstract MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC remains largely unknown. We investigated the function in human cell lines and patient tissue samples by experimental techniques in molecular biology including Co-IP assay, cell viability assay, quantitative real-time-PCR, et al. In addition, datasets were used to verify the results by database analysis. Statistical analysis was performed by using the GraphPad Prism 6 (GraphPad Software Inc., USA). A P value < 0.05 was defined as statistically significant. In this study, we found that miR-139 was significantly down-regulated in HCC. MiR-139 level was negatively associated with the stage of HCC, and HCC patients with higher miR-139 level had longer overall survival (OS) than these having lower miR-139 expression. Overexpression of miR-139 led to reduced cell viability, elevated apoptosis, and decreased colony forming, migratory and invasive capacities in HCC cells, while down-regulation of miR-139 led to opposite phenotypes. MiR-139 also inhibited HCC growth in a xenograft mouse model. We identified karyopherin alpha 2 (KPNA2) as a direct target of miR-139. KPNA2 is up-regulated in HCC and higher KPNA2 level is associated with poor patient prognosis. Silencing of KPNA2 expression led to similar phenotypic changes as miR-139 overexpression. Restoration of KPNA2 attenuated the suppressive effects of miR-139 overexpression on cell viability, apoptosis, colony formation, migration and invasion. In addition, miR-139 overexpression and KPNA2 depletion led to decreased nucleus level of POU class 5 homeobox 1 (POU5F1) and c-myc, two well-known pro-oncogenes. In together, these data revealed the essential roles of the miR-139/KPNA2 axis in HCC.
AbstractList Background MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC remains largely unknown. Methods We investigated the function in human cell lines and patient tissue samples by experimental techniques in molecular biology including Co-IP assay, cell viability assay, quantitative real-time-PCR, et al. In addition, datasets were used to verify the results by database analysis. Statistical analysis was performed by using the GraphPad Prism 6 (GraphPad Software Inc., USA). A P value < 0.05 was defined as statistically significant. Results In this study, we found that miR-139 was significantly down-regulated in HCC. MiR-139 level was negatively associated with the stage of HCC, and HCC patients with higher miR-139 level had longer overall survival (OS) than these having lower miR-139 expression. Overexpression of miR-139 led to reduced cell viability, elevated apoptosis, and decreased colony forming, migratory and invasive capacities in HCC cells, while down-regulation of miR-139 led to opposite phenotypes. MiR-139 also inhibited HCC growth in a xenograft mouse model. We identified karyopherin alpha 2 (KPNA2) as a direct target of miR-139. KPNA2 is up-regulated in HCC and higher KPNA2 level is associated with poor patient prognosis. Silencing of KPNA2 expression led to similar phenotypic changes as miR-139 overexpression. Restoration of KPNA2 attenuated the suppressive effects of miR-139 overexpression on cell viability, apoptosis, colony formation, migration and invasion. In addition, miR-139 overexpression and KPNA2 depletion led to decreased nucleus level of POU class 5 homeobox 1 (POU5F1) and c-myc, two well-known pro-oncogenes. Conclusion In together, these data revealed the essential roles of the miR-139/KPNA2 axis in HCC. Keywords: Survival, Epithelial-to-mesenchymal transition, Colony formation, Migration and invasion
Background MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC remains largely unknown. Methods We investigated the function in human cell lines and patient tissue samples by experimental techniques in molecular biology including Co-IP assay, cell viability assay, quantitative real-time-PCR, et al. In addition, datasets were used to verify the results by database analysis. Statistical analysis was performed by using the GraphPad Prism 6 (GraphPad Software Inc., USA). A P value < 0.05 was defined as statistically significant. Results In this study, we found that miR-139 was significantly down-regulated in HCC. MiR-139 level was negatively associated with the stage of HCC, and HCC patients with higher miR-139 level had longer overall survival (OS) than these having lower miR-139 expression. Overexpression of miR-139 led to reduced cell viability, elevated apoptosis, and decreased colony forming, migratory and invasive capacities in HCC cells, while down-regulation of miR-139 led to opposite phenotypes. MiR-139 also inhibited HCC growth in a xenograft mouse model. We identified karyopherin alpha 2 (KPNA2) as a direct target of miR-139. KPNA2 is up-regulated in HCC and higher KPNA2 level is associated with poor patient prognosis. Silencing of KPNA2 expression led to similar phenotypic changes as miR-139 overexpression. Restoration of KPNA2 attenuated the suppressive effects of miR-139 overexpression on cell viability, apoptosis, colony formation, migration and invasion. In addition, miR-139 overexpression and KPNA2 depletion led to decreased nucleus level of POU class 5 homeobox 1 (POU5F1) and c-myc, two well-known pro-oncogenes. Conclusion In together, these data revealed the essential roles of the miR-139/KPNA2 axis in HCC.
Abstract Background MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC remains largely unknown. Methods We investigated the function in human cell lines and patient tissue samples by experimental techniques in molecular biology including Co-IP assay, cell viability assay, quantitative real-time-PCR, et al. In addition, datasets were used to verify the results by database analysis. Statistical analysis was performed by using the GraphPad Prism 6 (GraphPad Software Inc., USA). A P value < 0.05 was defined as statistically significant. Results In this study, we found that miR-139 was significantly down-regulated in HCC. MiR-139 level was negatively associated with the stage of HCC, and HCC patients with higher miR-139 level had longer overall survival (OS) than these having lower miR-139 expression. Overexpression of miR-139 led to reduced cell viability, elevated apoptosis, and decreased colony forming, migratory and invasive capacities in HCC cells, while down-regulation of miR-139 led to opposite phenotypes. MiR-139 also inhibited HCC growth in a xenograft mouse model. We identified karyopherin alpha 2 (KPNA2) as a direct target of miR-139. KPNA2 is up-regulated in HCC and higher KPNA2 level is associated with poor patient prognosis. Silencing of KPNA2 expression led to similar phenotypic changes as miR-139 overexpression. Restoration of KPNA2 attenuated the suppressive effects of miR-139 overexpression on cell viability, apoptosis, colony formation, migration and invasion. In addition, miR-139 overexpression and KPNA2 depletion led to decreased nucleus level of POU class 5 homeobox 1 (POU5F1) and c-myc, two well-known pro-oncogenes. Conclusion In together, these data revealed the essential roles of the miR-139/KPNA2 axis in HCC.
MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC remains largely unknown. We investigated the function in human cell lines and patient tissue samples by experimental techniques in molecular biology including Co-IP assay, cell viability assay, quantitative real-time-PCR, et al. In addition, datasets were used to verify the results by database analysis. Statistical analysis was performed by using the GraphPad Prism 6 (GraphPad Software Inc., USA). A P value < 0.05 was defined as statistically significant. In this study, we found that miR-139 was significantly down-regulated in HCC. MiR-139 level was negatively associated with the stage of HCC, and HCC patients with higher miR-139 level had longer overall survival (OS) than these having lower miR-139 expression. Overexpression of miR-139 led to reduced cell viability, elevated apoptosis, and decreased colony forming, migratory and invasive capacities in HCC cells, while down-regulation of miR-139 led to opposite phenotypes. MiR-139 also inhibited HCC growth in a xenograft mouse model. We identified karyopherin alpha 2 (KPNA2) as a direct target of miR-139. KPNA2 is up-regulated in HCC and higher KPNA2 level is associated with poor patient prognosis. Silencing of KPNA2 expression led to similar phenotypic changes as miR-139 overexpression. Restoration of KPNA2 attenuated the suppressive effects of miR-139 overexpression on cell viability, apoptosis, colony formation, migration and invasion. In addition, miR-139 overexpression and KPNA2 depletion led to decreased nucleus level of POU class 5 homeobox 1 (POU5F1) and c-myc, two well-known pro-oncogenes. In together, these data revealed the essential roles of the miR-139/KPNA2 axis in HCC.
MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC remains largely unknown.BACKGROUNDMicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC remains largely unknown.We investigated the function in human cell lines and patient tissue samples by experimental techniques in molecular biology including Co-IP assay, cell viability assay, quantitative real-time-PCR, et al. In addition, datasets were used to verify the results by database analysis. Statistical analysis was performed by using the GraphPad Prism 6 (GraphPad Software Inc., USA). A P value < 0.05 was defined as statistically significant.METHODSWe investigated the function in human cell lines and patient tissue samples by experimental techniques in molecular biology including Co-IP assay, cell viability assay, quantitative real-time-PCR, et al. In addition, datasets were used to verify the results by database analysis. Statistical analysis was performed by using the GraphPad Prism 6 (GraphPad Software Inc., USA). A P value < 0.05 was defined as statistically significant.In this study, we found that miR-139 was significantly down-regulated in HCC. MiR-139 level was negatively associated with the stage of HCC, and HCC patients with higher miR-139 level had longer overall survival (OS) than these having lower miR-139 expression. Overexpression of miR-139 led to reduced cell viability, elevated apoptosis, and decreased colony forming, migratory and invasive capacities in HCC cells, while down-regulation of miR-139 led to opposite phenotypes. MiR-139 also inhibited HCC growth in a xenograft mouse model. We identified karyopherin alpha 2 (KPNA2) as a direct target of miR-139. KPNA2 is up-regulated in HCC and higher KPNA2 level is associated with poor patient prognosis. Silencing of KPNA2 expression led to similar phenotypic changes as miR-139 overexpression. Restoration of KPNA2 attenuated the suppressive effects of miR-139 overexpression on cell viability, apoptosis, colony formation, migration and invasion. In addition, miR-139 overexpression and KPNA2 depletion led to decreased nucleus level of POU class 5 homeobox 1 (POU5F1) and c-myc, two well-known pro-oncogenes.RESULTSIn this study, we found that miR-139 was significantly down-regulated in HCC. MiR-139 level was negatively associated with the stage of HCC, and HCC patients with higher miR-139 level had longer overall survival (OS) than these having lower miR-139 expression. Overexpression of miR-139 led to reduced cell viability, elevated apoptosis, and decreased colony forming, migratory and invasive capacities in HCC cells, while down-regulation of miR-139 led to opposite phenotypes. MiR-139 also inhibited HCC growth in a xenograft mouse model. We identified karyopherin alpha 2 (KPNA2) as a direct target of miR-139. KPNA2 is up-regulated in HCC and higher KPNA2 level is associated with poor patient prognosis. Silencing of KPNA2 expression led to similar phenotypic changes as miR-139 overexpression. Restoration of KPNA2 attenuated the suppressive effects of miR-139 overexpression on cell viability, apoptosis, colony formation, migration and invasion. In addition, miR-139 overexpression and KPNA2 depletion led to decreased nucleus level of POU class 5 homeobox 1 (POU5F1) and c-myc, two well-known pro-oncogenes.In together, these data revealed the essential roles of the miR-139/KPNA2 axis in HCC.CONCLUSIONIn together, these data revealed the essential roles of the miR-139/KPNA2 axis in HCC.
MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC remains largely unknown. We investigated the function in human cell lines and patient tissue samples by experimental techniques in molecular biology including Co-IP assay, cell viability assay, quantitative real-time-PCR, et al. In addition, datasets were used to verify the results by database analysis. Statistical analysis was performed by using the GraphPad Prism 6 (GraphPad Software Inc., USA). A P value < 0.05 was defined as statistically significant. In this study, we found that miR-139 was significantly down-regulated in HCC. MiR-139 level was negatively associated with the stage of HCC, and HCC patients with higher miR-139 level had longer overall survival (OS) than these having lower miR-139 expression. Overexpression of miR-139 led to reduced cell viability, elevated apoptosis, and decreased colony forming, migratory and invasive capacities in HCC cells, while down-regulation of miR-139 led to opposite phenotypes. MiR-139 also inhibited HCC growth in a xenograft mouse model. We identified karyopherin alpha 2 (KPNA2) as a direct target of miR-139. KPNA2 is up-regulated in HCC and higher KPNA2 level is associated with poor patient prognosis. Silencing of KPNA2 expression led to similar phenotypic changes as miR-139 overexpression. Restoration of KPNA2 attenuated the suppressive effects of miR-139 overexpression on cell viability, apoptosis, colony formation, migration and invasion. In addition, miR-139 overexpression and KPNA2 depletion led to decreased nucleus level of POU class 5 homeobox 1 (POU5F1) and c-myc, two well-known pro-oncogenes. In together, these data revealed the essential roles of the miR-139/KPNA2 axis in HCC.
ArticleNumber 182
Audience Academic
Author Liang, Liang
Tian, Tian
Zan, Ying
Dong, Lei
Dai, Zhijun
Deng, Yujiao
Wang, Baofeng
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/31046781$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1002/jso.24114
10.4254/wjh.v9.i23.1001
10.2174/1566523214666141224095610
10.1038/cddis.2013.256
10.1186/s12885-015-1369-8
10.1158/1078-0432.CCR-05-2090
10.1038/s41388-017-0057-3
10.1038/sj.onc.1209283
10.1038/nmeth.1608
10.1007/s13277-015-3199-3
10.1002/jcp.26607
10.1038/nrc.2017.118
10.1016/S0140-6736(11)61347-0
10.1053/j.gastro.2011.08.050
10.1053/j.gastro.2004.09.036
10.3892/or.2013.2831
10.1002/cam4.505
10.18632/oncotarget.21791
10.1038/bjc.2015.165
10.18632/oncotarget.16749
10.1053/j.gastro.2010.10.006
10.1007/s11060-012-0924-2
10.1097/00004836-200211002-00009
10.1002/hep.22160
10.1080/15548627.2015.1108507
10.1002/cbf.2902
10.1002/path.4390
10.1038/srep27157
10.1016/j.cell.2010.03.009
10.1016/j.bbrc.2015.05.062
10.3390/ijms19041115
10.1016/0014-4827(92)90012-W
10.1038/s41389-017-0008-4
10.1097/MCG.0b013e3182872f29
10.1186/gb-2014-15-1-r9
10.1016/j.lfs.2017.10.010
10.1080/15384047.2018.1423922
10.1261/rna.042143.113
10.1016/j.canlet.2012.12.013
10.1038/onc.2009.211
10.18632/oncotarget.4363
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Issue 1
Keywords Migration and invasion
Colony formation
Survival
Epithelial-to-mesenchymal transition
Language English
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References 1175_CR37
AA Mohamed (1175_CR27) 2017; 9
C Coulouarn (1175_CR8) 2009; 28
E Dahl (1175_CR41) 2006; 12
W Gu (1175_CR11) 2014; 31
Q Li (1175_CR29) 2016; 6
T Takada (1175_CR16) 2016; 113
Y Hu (1175_CR34) 2017; 8
Z H-d (1175_CR35) 2015; 36
T Brabletz (1175_CR39) 2018; 18
A Budhu (1175_CR7) 2008; 47
W Bao (1175_CR32) 2011; 141
G Qiu (1175_CR13) 2015; 463
M Henriksson (1175_CR42) 1992; 203
Y Yang (1175_CR23) 2017; 8
S Thakral (1175_CR9) 2015; 15
BI Carr (1175_CR4) 2004; 127
TA Farazi (1175_CR26) 2014; 15
K Ikenberg (1175_CR19) 2014; 234
L Huang (1175_CR18) 2013; 4
CL Gao (1175_CR22) 2018; 15
S Hua (1175_CR38) 2018; 37
A Christiansen (1175_CR14) 2013; 331
L Mourad (1175_CR43) 2018; 19
A Forner (1175_CR2) 2012; 379
Q Fan (1175_CR31) 2013; 31
AT Alshareeda (1175_CR15) 2015; 112
S Kishore (1175_CR25) 2011; 8
C Cha (1175_CR1) 2002; 35
X Yu (1175_CR36) 2018; 15
S Mittal (1175_CR3) 2013; 47
Y Lu (1175_CR21) 2015; 11
M Hafner (1175_CR24) 2010; 141
K Watanabe (1175_CR33) 2015; 4
Y Murakami (1175_CR6) 2005; 25
J Lin (1175_CR20) 2015; 6
Z Bian (1175_CR30) 2017; 6
K Krishnan (1175_CR10) 2013; 19
B Shi (1175_CR17) 2015; 15
1175_CR5
K Gousias (1175_CR40) 2012; 109
CC Wong (1175_CR12) 2011; 140
C Zhong (1175_CR28) 2017; 191
References_xml – volume: 113
  start-page: 213
  issue: 2
  year: 2016
  ident: 1175_CR16
  publication-title: J Surg Oncol
  doi: 10.1002/jso.24114
– volume: 9
  start-page: 1001
  issue: 23
  year: 2017
  ident: 1175_CR27
  publication-title: World J Hepatol
  doi: 10.4254/wjh.v9.i23.1001
– volume: 15
  start-page: 142
  issue: 2
  year: 2015
  ident: 1175_CR9
  publication-title: Current gene therapy
  doi: 10.2174/1566523214666141224095610
– volume: 4
  start-page: e745
  year: 2013
  ident: 1175_CR18
  publication-title: Cell Death Dis
  doi: 10.1038/cddis.2013.256
– volume: 15
  start-page: 380
  year: 2015
  ident: 1175_CR17
  publication-title: BMC Cancer
  doi: 10.1186/s12885-015-1369-8
– volume: 12
  start-page: 3950
  issue: 13
  year: 2006
  ident: 1175_CR41
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-05-2090
– volume: 37
  start-page: 1624
  issue: 12
  year: 2018
  ident: 1175_CR38
  publication-title: Oncogene.
  doi: 10.1038/s41388-017-0057-3
– volume: 25
  start-page: 2537
  year: 2005
  ident: 1175_CR6
  publication-title: Oncogene.
  doi: 10.1038/sj.onc.1209283
– volume: 8
  start-page: 559
  issue: 7
  year: 2011
  ident: 1175_CR25
  publication-title: Nat Methods
  doi: 10.1038/nmeth.1608
– volume: 36
  start-page: 1355
  issue: 3
  year: 2015
  ident: 1175_CR35
  publication-title: Tumor Biol
  doi: 10.1007/s13277-015-3199-3
– ident: 1175_CR5
  doi: 10.1002/jcp.26607
– volume: 18
  start-page: 128
  issue: 2
  year: 2018
  ident: 1175_CR39
  publication-title: Nat Rev Cancer
  doi: 10.1038/nrc.2017.118
– volume: 379
  start-page: 1245
  issue: 9822
  year: 2012
  ident: 1175_CR2
  publication-title: Lancet
  doi: 10.1016/S0140-6736(11)61347-0
– volume: 141
  start-page: 2076
  issue: 6
  year: 2011
  ident: 1175_CR32
  publication-title: Gastroenterology.
  doi: 10.1053/j.gastro.2011.08.050
– volume: 127
  start-page: S218
  issue: 5 Suppl 1
  year: 2004
  ident: 1175_CR4
  publication-title: Gastroenterology.
  doi: 10.1053/j.gastro.2004.09.036
– volume: 31
  start-page: 397
  issue: 1
  year: 2014
  ident: 1175_CR11
  publication-title: Oncol Rep
  doi: 10.3892/or.2013.2831
– volume: 4
  start-page: 1573
  issue: 10
  year: 2015
  ident: 1175_CR33
  publication-title: Cancer medicine
  doi: 10.1002/cam4.505
– volume: 8
  start-page: 94554
  issue: 55
  year: 2017
  ident: 1175_CR34
  publication-title: Oncotarget.
  doi: 10.18632/oncotarget.21791
– volume: 112
  start-page: 1929
  issue: 12
  year: 2015
  ident: 1175_CR15
  publication-title: Br J Cancer
  doi: 10.1038/bjc.2015.165
– volume: 8
  start-page: 36289
  issue: 22
  year: 2017
  ident: 1175_CR23
  publication-title: Oncotarget.
  doi: 10.18632/oncotarget.16749
– volume: 140
  start-page: 322
  issue: 1
  year: 2011
  ident: 1175_CR12
  publication-title: Gastroenterology.
  doi: 10.1053/j.gastro.2010.10.006
– volume: 15
  start-page: 5977
  issue: 4
  year: 2018
  ident: 1175_CR36
  publication-title: Oncol Lett
– volume: 109
  start-page: 545
  issue: 3
  year: 2012
  ident: 1175_CR40
  publication-title: J Neuro-Oncol
  doi: 10.1007/s11060-012-0924-2
– volume: 35
  start-page: S130
  issue: 5 Suppl 2
  year: 2002
  ident: 1175_CR1
  publication-title: J Clin Gastroenterol
  doi: 10.1097/00004836-200211002-00009
– volume: 47
  start-page: 897
  issue: 3
  year: 2008
  ident: 1175_CR7
  publication-title: Hepatology (Baltimore, Md)
  doi: 10.1002/hep.22160
– volume: 11
  start-page: 2213
  issue: 12
  year: 2015
  ident: 1175_CR21
  publication-title: Autophagy.
  doi: 10.1080/15548627.2015.1108507
– volume: 31
  start-page: 319
  issue: 4
  year: 2013
  ident: 1175_CR31
  publication-title: Cell Biochem Funct
  doi: 10.1002/cbf.2902
– volume: 234
  start-page: 239
  issue: 2
  year: 2014
  ident: 1175_CR19
  publication-title: J Pathol
  doi: 10.1002/path.4390
– volume: 6
  year: 2016
  ident: 1175_CR29
  publication-title: Sci Rep
  doi: 10.1038/srep27157
– volume: 15
  start-page: 2815
  issue: 3
  year: 2018
  ident: 1175_CR22
  publication-title: Oncol Lett
– volume: 141
  start-page: 129
  issue: 1
  year: 2010
  ident: 1175_CR24
  publication-title: Cell.
  doi: 10.1016/j.cell.2010.03.009
– volume: 463
  start-page: 315
  issue: 3
  year: 2015
  ident: 1175_CR13
  publication-title: Biochem Biophys Res Commun
  doi: 10.1016/j.bbrc.2015.05.062
– ident: 1175_CR37
  doi: 10.3390/ijms19041115
– volume: 203
  start-page: 383
  issue: 2
  year: 1992
  ident: 1175_CR42
  publication-title: Exp Cell Res
  doi: 10.1016/0014-4827(92)90012-W
– volume: 6
  start-page: 395
  issue: 11
  year: 2017
  ident: 1175_CR30
  publication-title: Oncogenesis.
  doi: 10.1038/s41389-017-0008-4
– volume: 47
  start-page: S2
  year: 2013
  ident: 1175_CR3
  publication-title: J Clin Gastroenterol
  doi: 10.1097/MCG.0b013e3182872f29
– volume: 15
  start-page: R9
  issue: 1
  year: 2014
  ident: 1175_CR26
  publication-title: Genome Biol
  doi: 10.1186/gb-2014-15-1-r9
– volume: 191
  start-page: 68
  year: 2017
  ident: 1175_CR28
  publication-title: Life Sci
  doi: 10.1016/j.lfs.2017.10.010
– volume: 19
  start-page: 400
  issue: 5
  year: 2018
  ident: 1175_CR43
  publication-title: Cancer Biol Ther
  doi: 10.1080/15384047.2018.1423922
– volume: 19
  start-page: 1767
  issue: 12
  year: 2013
  ident: 1175_CR10
  publication-title: RNA (New York, NY)
  doi: 10.1261/rna.042143.113
– volume: 331
  start-page: 18
  issue: 1
  year: 2013
  ident: 1175_CR14
  publication-title: Cancer Lett
  doi: 10.1016/j.canlet.2012.12.013
– volume: 28
  start-page: 3526
  issue: 40
  year: 2009
  ident: 1175_CR8
  publication-title: Oncogene.
  doi: 10.1038/onc.2009.211
– volume: 6
  start-page: 23793
  issue: 27
  year: 2015
  ident: 1175_CR20
  publication-title: Oncotarget.
  doi: 10.18632/oncotarget.4363
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Snippet MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC...
Background MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of...
Abstract Background MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact...
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StartPage 182
SubjectTerms Analysis
Apoptosis
Binding sites
Biomarkers
Breast cancer
Cancer
Cancer therapies
Carcinoma
Care and treatment
Cell cycle
Cell growth
Cells (Biology)
Colony formation
Colorectal cancer
Development and progression
Epithelial-to-mesenchymal transition
Gastric cancer
Gene expression
Genetic aspects
Growth
Hepatocellular carcinoma
Kinases
Liver cancer
Medical prognosis
Metastasis
MicroRNA
MicroRNAs
Migration and invasion
Molecular biology
Patients
Phenotypes
Physiological aspects
Proteins
Roles
Statistics
Stem cells
Studies
Surgery
Survival
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Title MicroRNA-139 inhibits hepatocellular carcinoma cell growth through down-regulating karyopherin alpha 2
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