Establishing of mouse oral carcinoma cell lines derived from transgenic mice and their use as syngeneic tumorigenesis models

Background The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP- miR-211 transgenic mice also exhibit augmented potential for OSCC induction. Methods Four murine OSCC cell...

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Published inBMC cancer Vol. 19; no. 1; pp. 281 - 11
Main Authors Chen, Yi-Fen, Liu, Chung-Ji, Lin, Li-Han, Chou, Chung-Hsien, Yeh, Li-Yin, Lin, Shu-Chun, Chang, Kuo-Wei
Format Journal Article
LanguageEnglish
Published London BioMed Central 29.03.2019
BioMed Central Ltd
BMC
Subjects
4-Nitroquinoline 1-oxide
Analysis
Animal models
Biomedical and Life Sciences
Biomedicine
Breast cancer
Cancer
Cancer metastasis
Cancer Research
Carcinogenesis
Carcinoma
Cell adhesion & migration
Cell and molecular biology
Cell growth
Cell lines
Cisplatin
Deoxyribonucleic acid
Dermis
DNA
DNA binding
Fluorescence
Genes
Genetic aspects
Genetic engineering
Genetically modified organisms
Head & neck cancer
Health Promotion and Disease Prevention
House mouse
Medicine/Public Health
Mesenchyme
Metastases
Metastasis
MicroRNA
miR-211
Missense mutation
Mouse
Mouth cancer
Oncology
Oral cancer
Oral carcinoma
Oxidative stress
p53 Protein
Pathogenesis
Patients
Research Article
Stem cells
Surgical Oncology
Tongue
Transgenic animals
Transgenic mice
Tumor cell lines
Tumor proteins
Tumorigenesis
Tumors
Xenografts
Oral carcinoma
microRNA
Tongue
Mouse
miR-211
Online AccessGet full text
ISSN1471-2407
1471-2407
DOI10.1186/s12885-019-5486-7

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Abstract Background The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP- miR-211 transgenic mice also exhibit augmented potential for OSCC induction. Methods Four murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP- miR-211 transgenic mouse model. The genetic disruption, in vitro oncogenicity, and the eligibilities of tumorigenesis and metastasis of the cell lines are analyzed. Results All cell lines show green fluorescence and express a range of epithelial markers. The MOC-L1, MOC-L2 and MOC-L3 cells carry missense mutations in the DNA binding domain of the p53 gene. MOC-L1 exhibits a high level of epithelial-mesenchymal transition and has the aggressive characteristics associated with this. MOC-L1 and MOC-L2 are clonogenic in vitro as well as being tumorigenic when implanted into the dermis or tongue of syngeneic recipients. Nonetheless, only MOC-L1 exhibits immense potential for local regional and distal metastasis. Since the expression of miR-196b in MOC-L1 xenografts is drastically decreased on cisplatin treatment, it would seem that targeting of miR-196b might facilitate tumor abrogation. Conclusions As cell lines established in this study originated from the C57BL/6 mouse, the strain most suitable for transgenic engineering, exploring the interplay of these OSCC cells with other genetically modified cells in immune-competent mice would provide important insights into OSCC pathogenesis.
AbstractList The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP-miR-211 transgenic mice also exhibit augmented potential for OSCC induction.BACKGROUNDThe survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP-miR-211 transgenic mice also exhibit augmented potential for OSCC induction.Four murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP-miR-211 transgenic mouse model. The genetic disruption, in vitro oncogenicity, and the eligibilities of tumorigenesis and metastasis of the cell lines are analyzed.METHODSFour murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP-miR-211 transgenic mouse model. The genetic disruption, in vitro oncogenicity, and the eligibilities of tumorigenesis and metastasis of the cell lines are analyzed.All cell lines show green fluorescence and express a range of epithelial markers. The MOC-L1, MOC-L2 and MOC-L3 cells carry missense mutations in the DNA binding domain of the p53 gene. MOC-L1 exhibits a high level of epithelial-mesenchymal transition and has the aggressive characteristics associated with this. MOC-L1 and MOC-L2 are clonogenic in vitro as well as being tumorigenic when implanted into the dermis or tongue of syngeneic recipients. Nonetheless, only MOC-L1 exhibits immense potential for local regional and distal metastasis. Since the expression of miR-196b in MOC-L1 xenografts is drastically decreased on cisplatin treatment, it would seem that targeting of miR-196b might facilitate tumor abrogation.RESULTSAll cell lines show green fluorescence and express a range of epithelial markers. The MOC-L1, MOC-L2 and MOC-L3 cells carry missense mutations in the DNA binding domain of the p53 gene. MOC-L1 exhibits a high level of epithelial-mesenchymal transition and has the aggressive characteristics associated with this. MOC-L1 and MOC-L2 are clonogenic in vitro as well as being tumorigenic when implanted into the dermis or tongue of syngeneic recipients. Nonetheless, only MOC-L1 exhibits immense potential for local regional and distal metastasis. Since the expression of miR-196b in MOC-L1 xenografts is drastically decreased on cisplatin treatment, it would seem that targeting of miR-196b might facilitate tumor abrogation.As cell lines established in this study originated from the C57BL/6 mouse, the strain most suitable for transgenic engineering, exploring the interplay of these OSCC cells with other genetically modified cells in immune-competent mice would provide important insights into OSCC pathogenesis.CONCLUSIONSAs cell lines established in this study originated from the C57BL/6 mouse, the strain most suitable for transgenic engineering, exploring the interplay of these OSCC cells with other genetically modified cells in immune-competent mice would provide important insights into OSCC pathogenesis.
The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP-miR-211 transgenic mice also exhibit augmented potential for OSCC induction. Four murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP-miR-211 transgenic mouse model. The genetic disruption, in vitro oncogenicity, and the eligibilities of tumorigenesis and metastasis of the cell lines are analyzed. All cell lines show green fluorescence and express a range of epithelial markers. The MOC-L1, MOC-L2 and MOC-L3 cells carry missense mutations in the DNA binding domain of the p53 gene. MOC-L1 exhibits a high level of epithelial-mesenchymal transition and has the aggressive characteristics associated with this. MOC-L1 and MOC-L2 are clonogenic in vitro as well as being tumorigenic when implanted into the dermis or tongue of syngeneic recipients. Nonetheless, only MOC-L1 exhibits immense potential for local regional and distal metastasis. Since the expression of miR-196b in MOC-L1 xenografts is drastically decreased on cisplatin treatment, it would seem that targeting of miR-196b might facilitate tumor abrogation. As cell lines established in this study originated from the C57BL/6 mouse, the strain most suitable for transgenic engineering, exploring the interplay of these OSCC cells with other genetically modified cells in immune-competent mice would provide important insights into OSCC pathogenesis.
Background The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP-miR-211 transgenic mice also exhibit augmented potential for OSCC induction. Methods Four murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP-miR-211 transgenic mouse model. The genetic disruption, in vitro oncogenicity, and the eligibilities of tumorigenesis and metastasis of the cell lines are analyzed. Results All cell lines show green fluorescence and express a range of epithelial markers. The MOC-L1, MOC-L2 and MOC-L3 cells carry missense mutations in the DNA binding domain of the p53 gene. MOC-L1 exhibits a high level of epithelial-mesenchymal transition and has the aggressive characteristics associated with this. MOC-L1 and MOC-L2 are clonogenic in vitro as well as being tumorigenic when implanted into the dermis or tongue of syngeneic recipients. Nonetheless, only MOC-L1 exhibits immense potential for local regional and distal metastasis. Since the expression of miR-196b in MOC-L1 xenografts is drastically decreased on cisplatin treatment, it would seem that targeting of miR-196b might facilitate tumor abrogation. Conclusions As cell lines established in this study originated from the C57BL/6 mouse, the strain most suitable for transgenic engineering, exploring the interplay of these OSCC cells with other genetically modified cells in immune-competent mice would provide important insights into OSCC pathogenesis. Keywords: Mouse, microRNA, miR-211, Oral carcinoma, Tongue
The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP-miR-211 transgenic mice also exhibit augmented potential for OSCC induction. Four murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP-miR-211 transgenic mouse model. The genetic disruption, in vitro oncogenicity, and the eligibilities of tumorigenesis and metastasis of the cell lines are analyzed. All cell lines show green fluorescence and express a range of epithelial markers. The MOC-L1, MOC-L2 and MOC-L3 cells carry missense mutations in the DNA binding domain of the p53 gene. MOC-L1 exhibits a high level of epithelial-mesenchymal transition and has the aggressive characteristics associated with this. MOC-L1 and MOC-L2 are clonogenic in vitro as well as being tumorigenic when implanted into the dermis or tongue of syngeneic recipients. Nonetheless, only MOC-L1 exhibits immense potential for local regional and distal metastasis. Since the expression of miR-196b in MOC-L1 xenografts is drastically decreased on cisplatin treatment, it would seem that targeting of miR-196b might facilitate tumor abrogation. As cell lines established in this study originated from the C57BL/6 mouse, the strain most suitable for transgenic engineering, exploring the interplay of these OSCC cells with other genetically modified cells in immune-competent mice would provide important insights into OSCC pathogenesis.
Background The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP-miR-211 transgenic mice also exhibit augmented potential for OSCC induction. Methods Four murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP-miR-211 transgenic mouse model. The genetic disruption, in vitro oncogenicity, and the eligibilities of tumorigenesis and metastasis of the cell lines are analyzed. Results All cell lines show green fluorescence and express a range of epithelial markers. The MOC-L1, MOC-L2 and MOC-L3 cells carry missense mutations in the DNA binding domain of the p53 gene. MOC-L1 exhibits a high level of epithelial-mesenchymal transition and has the aggressive characteristics associated with this. MOC-L1 and MOC-L2 are clonogenic in vitro as well as being tumorigenic when implanted into the dermis or tongue of syngeneic recipients. Nonetheless, only MOC-L1 exhibits immense potential for local regional and distal metastasis. Since the expression of miR-196b in MOC-L1 xenografts is drastically decreased on cisplatin treatment, it would seem that targeting of miR-196b might facilitate tumor abrogation. Conclusions As cell lines established in this study originated from the C57BL/6 mouse, the strain most suitable for transgenic engineering, exploring the interplay of these OSCC cells with other genetically modified cells in immune-competent mice would provide important insights into OSCC pathogenesis.
Abstract Background The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP-miR-211 transgenic mice also exhibit augmented potential for OSCC induction. Methods Four murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP-miR-211 transgenic mouse model. The genetic disruption, in vitro oncogenicity, and the eligibilities of tumorigenesis and metastasis of the cell lines are analyzed. Results All cell lines show green fluorescence and express a range of epithelial markers. The MOC-L1, MOC-L2 and MOC-L3 cells carry missense mutations in the DNA binding domain of the p53 gene. MOC-L1 exhibits a high level of epithelial-mesenchymal transition and has the aggressive characteristics associated with this. MOC-L1 and MOC-L2 are clonogenic in vitro as well as being tumorigenic when implanted into the dermis or tongue of syngeneic recipients. Nonetheless, only MOC-L1 exhibits immense potential for local regional and distal metastasis. Since the expression of miR-196b in MOC-L1 xenografts is drastically decreased on cisplatin treatment, it would seem that targeting of miR-196b might facilitate tumor abrogation. Conclusions As cell lines established in this study originated from the C57BL/6 mouse, the strain most suitable for transgenic engineering, exploring the interplay of these OSCC cells with other genetically modified cells in immune-competent mice would provide important insights into OSCC pathogenesis.
Background The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor patient survival. K14-EGFP- miR-211 transgenic mice also exhibit augmented potential for OSCC induction. Methods Four murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP- miR-211 transgenic mouse model. The genetic disruption, in vitro oncogenicity, and the eligibilities of tumorigenesis and metastasis of the cell lines are analyzed. Results All cell lines show green fluorescence and express a range of epithelial markers. The MOC-L1, MOC-L2 and MOC-L3 cells carry missense mutations in the DNA binding domain of the p53 gene. MOC-L1 exhibits a high level of epithelial-mesenchymal transition and has the aggressive characteristics associated with this. MOC-L1 and MOC-L2 are clonogenic in vitro as well as being tumorigenic when implanted into the dermis or tongue of syngeneic recipients. Nonetheless, only MOC-L1 exhibits immense potential for local regional and distal metastasis. Since the expression of miR-196b in MOC-L1 xenografts is drastically decreased on cisplatin treatment, it would seem that targeting of miR-196b might facilitate tumor abrogation. Conclusions As cell lines established in this study originated from the C57BL/6 mouse, the strain most suitable for transgenic engineering, exploring the interplay of these OSCC cells with other genetically modified cells in immune-competent mice would provide important insights into OSCC pathogenesis.
ArticleNumber 281
Audience Academic
Author Chou, Chung-Hsien
Chang, Kuo-Wei
Chen, Yi-Fen
Liu, Chung-Ji
Lin, Li-Han
Yeh, Li-Yin
Lin, Shu-Chun
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/30922255$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1534/g3.114.014712
10.1016/j.canlet.2013.05.032
10.7150/jca.13460
10.1002/hed.2880160506
10.1002/(SICI)1520-6823(1999)7:1<22::AID-ROI3>3.0.CO;2-6
10.1016/j.redox.2019.101140
10.1002/ijc.29106
10.1186/1472-6750-11-124
10.1245/s10434-012-2618-6
10.1364/BOE.9.001461
10.1016/j.oraloncology.2008.06.002
10.1038/s41467-018-04070-6
10.1016/j.redox.2018.101080
10.1002/(SICI)1097-0215(19990730)82:3<377::AID-IJC11>3.0.CO;2-9
10.3892/ol.2016.4491
10.1038/cdd.2017.180
10.1158/0008-5472.CAN-15-1664
10.1016/j.bbagrm.2015.06.014
10.1093/carcin/bgs023
10.1158/1538-7445.AM2015-4000
10.1016/j.oraloncology.2017.07.028
10.1002/jcb.27753
10.18632/oncotarget.2741
10.1158/0008-5472.CAN-17-0068
10.1186/1476-4598-9-238
10.1177/154405910808701116
10.1158/0008-5472.CAN-09-2291
10.1016/j.oraloncology.2018.10.018
10.14336/AD.2016.0118
10.1158/2326-6066.CIR-14-0205
10.1002/ijc.21694
10.1038/s41598-017-18138-8
10.1016/j.clinbiochem.2014.11.020
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Issue 1
Keywords Oral carcinoma
microRNA
Tongue
Mouse
miR-211
Language English
License Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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References YF Chen (5486_CR17) 2019; 22
S Fantini (5486_CR30) 2015; 1849
R Sumareva (5486_CR3) 1999; 7
PH Chen (5486_CR20) 2018; 9
S Liang (5486_CR24) 2015; 6
SY Alcoser (5486_CR22) 2011; 11
YC Lu (5486_CR29) 2016; 7
S Alvarez-Teijeiro (5486_CR6) 2017; 7
TH Chu (5486_CR8) 2013; 337
CJ Liu (5486_CR10) 2013; 20
SH Tseng (5486_CR18) 2015; 136
BL Hawkins (5486_CR19) 1994; 16
KW Chang (5486_CR14) 2008; 87
DJ Downes (5486_CR26) 2014; 4
LP Smith (5486_CR5) 2006; 118
YC Lu (5486_CR13) 2015; 48
GR Thomas (5486_CR4) 1999; 82
PP Reis (5486_CR12) 2010; 9
CJ Liu (5486_CR9) 2010; 70
S Ma (5486_CR32) 2016; 2016
L Vera-Ramirez (5486_CR28) 2018; 9
5486_CR15
EH Baugh (5486_CR25) 2018; 25
YS Ryu (5486_CR33) 2019; 21
MH Manjili (5486_CR27) 2017; 77
5486_CR11
YY Hou (5486_CR16) 2016; 11
K Ishida (5486_CR2) 2017; 73
N Tanaka (5486_CR34) 2018; 87
YF Chen (5486_CR7) 2016; 76
ZG Lei (5486_CR21) 2016; 9
YL Liao (5486_CR31) 2012; 33
JD Schoenfeld (5486_CR35) 2015; 3
L Ma (5486_CR23) 2016; 7
S Warnakulasuriya (5486_CR1) 2009; 45
References_xml – volume: 4
  start-page: 2483
  issue: 12
  year: 2014
  ident: 5486_CR26
  publication-title: G3 (Bethesda)
  doi: 10.1534/g3.114.014712
– volume: 9
  start-page: 545
  year: 2016
  ident: 5486_CR21
  publication-title: Onco Targets Ther
– volume: 2016
  start-page: 4693703
  year: 2016
  ident: 5486_CR32
  publication-title: Oxidative Med Cell Longev
– volume: 337
  start-page: 115
  issue: 1
  year: 2013
  ident: 5486_CR8
  publication-title: Cancer Lett
  doi: 10.1016/j.canlet.2013.05.032
– volume: 7
  start-page: 650
  issue: 6
  year: 2016
  ident: 5486_CR29
  publication-title: J Cancer
  doi: 10.7150/jca.13460
– volume: 16
  start-page: 424
  issue: 5
  year: 1994
  ident: 5486_CR19
  publication-title: Head Neck
  doi: 10.1002/hed.2880160506
– volume: 7
  start-page: 22
  issue: 1
  year: 1999
  ident: 5486_CR3
  publication-title: Radiat Oncol Investig
  doi: 10.1002/(SICI)1520-6823(1999)7:1<22::AID-ROI3>3.0.CO;2-6
– volume: 22
  year: 2019
  ident: 5486_CR17
  publication-title: Redox Biol
  doi: 10.1016/j.redox.2019.101140
– volume: 136
  start-page: 1263
  issue: 6
  year: 2015
  ident: 5486_CR18
  publication-title: Int J Cancer
  doi: 10.1002/ijc.29106
– volume: 11
  start-page: 124
  year: 2011
  ident: 5486_CR22
  publication-title: BMC Biotechnol
  doi: 10.1186/1472-6750-11-124
– volume: 20
  start-page: S406
  issue: Suppl 3
  year: 2013
  ident: 5486_CR10
  publication-title: Ann Surg Oncol
  doi: 10.1245/s10434-012-2618-6
– volume: 9
  start-page: 1461
  issue: 4
  year: 2018
  ident: 5486_CR20
  publication-title: Biomed Opt Express
  doi: 10.1364/BOE.9.001461
– volume: 45
  start-page: 309
  issue: 4–5
  year: 2009
  ident: 5486_CR1
  publication-title: Oral Oncol
  doi: 10.1016/j.oraloncology.2008.06.002
– volume: 9
  start-page: 1944
  issue: 1
  year: 2018
  ident: 5486_CR28
  publication-title: Nat Commun
  doi: 10.1038/s41467-018-04070-6
– volume: 21
  start-page: 101080
  year: 2019
  ident: 5486_CR33
  publication-title: Redox Biol
  doi: 10.1016/j.redox.2018.101080
– volume: 82
  start-page: 377
  issue: 3
  year: 1999
  ident: 5486_CR4
  publication-title: Int J Cancer
  doi: 10.1002/(SICI)1097-0215(19990730)82:3<377::AID-IJC11>3.0.CO;2-9
– volume: 11
  start-page: 4013
  issue: 6
  year: 2016
  ident: 5486_CR16
  publication-title: Oncol Lett
  doi: 10.3892/ol.2016.4491
– volume: 25
  start-page: 154
  issue: 1
  year: 2018
  ident: 5486_CR25
  publication-title: Cell Death Differ
  doi: 10.1038/cdd.2017.180
– volume: 76
  start-page: 4872
  issue: 16
  year: 2016
  ident: 5486_CR7
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-15-1664
– volume: 1849
  start-page: 1066
  issue: 8
  year: 2015
  ident: 5486_CR30
  publication-title: Biochim Biophys Acta
  doi: 10.1016/j.bbagrm.2015.06.014
– volume: 33
  start-page: 760
  issue: 4
  year: 2012
  ident: 5486_CR31
  publication-title: Carcinogenesis
  doi: 10.1093/carcin/bgs023
– ident: 5486_CR11
  doi: 10.1158/1538-7445.AM2015-4000
– volume: 73
  start-page: 16
  year: 2017
  ident: 5486_CR2
  publication-title: Oral Oncol
  doi: 10.1016/j.oraloncology.2017.07.028
– ident: 5486_CR15
  doi: 10.1002/jcb.27753
– volume: 6
  start-page: 1020
  issue: 2
  year: 2015
  ident: 5486_CR24
  publication-title: Oncotarget
  doi: 10.18632/oncotarget.2741
– volume: 77
  start-page: 2564
  issue: 10
  year: 2017
  ident: 5486_CR27
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-17-0068
– volume: 9
  start-page: 238
  year: 2010
  ident: 5486_CR12
  publication-title: Mol Cancer
  doi: 10.1186/1476-4598-9-238
– volume: 87
  start-page: 1063
  issue: 11
  year: 2008
  ident: 5486_CR14
  publication-title: J Dent Res
  doi: 10.1177/154405910808701116
– volume: 70
  start-page: 1635
  issue: 4
  year: 2010
  ident: 5486_CR9
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-09-2291
– volume: 87
  start-page: 49
  year: 2018
  ident: 5486_CR34
  publication-title: Oral Oncol
  doi: 10.1016/j.oraloncology.2018.10.018
– volume: 7
  start-page: 254
  issue: 3
  year: 2016
  ident: 5486_CR23
  publication-title: Aging Dis
  doi: 10.14336/AD.2016.0118
– volume: 3
  start-page: 12
  issue: 1
  year: 2015
  ident: 5486_CR35
  publication-title: Cancer Immunol Res
  doi: 10.1158/2326-6066.CIR-14-0205
– volume: 118
  start-page: 2111
  issue: 9
  year: 2006
  ident: 5486_CR5
  publication-title: Int J Cancer
  doi: 10.1002/ijc.21694
– volume: 7
  issue: 1
  year: 2017
  ident: 5486_CR6
  publication-title: Sci Rep
  doi: 10.1038/s41598-017-18138-8
– volume: 48
  start-page: 115
  issue: 3
  year: 2015
  ident: 5486_CR13
  publication-title: Clin Biochem
  doi: 10.1016/j.clinbiochem.2014.11.020
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Snippet Background The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression...
The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression and poor...
Background The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor progression...
Abstract Background The survival of OSCC patient needs to be further improved. miR-211 is oncogenic in OSCC and its upregulation is associated with tumor...
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SubjectTerms 4-Nitroquinoline 1-oxide
Analysis
Animal models
Biomedical and Life Sciences
Biomedicine
Breast cancer
Cancer
Cancer metastasis
Cancer Research
Carcinogenesis
Carcinoma
Cell adhesion & migration
Cell and molecular biology
Cell growth
Cell lines
Cisplatin
Deoxyribonucleic acid
Dermis
DNA
DNA binding
Fluorescence
Genes
Genetic aspects
Genetic engineering
Genetically modified organisms
Head & neck cancer
Health Promotion and Disease Prevention
House mouse
Medicine/Public Health
Mesenchyme
Metastases
Metastasis
MicroRNA
miR-211
Missense mutation
Mouse
Mouth cancer
Oncology
Oral cancer
Oral carcinoma
Oxidative stress
p53 Protein
Pathogenesis
Patients
Research Article
Stem cells
Surgical Oncology
Tongue
Transgenic animals
Transgenic mice
Tumor cell lines
Tumor proteins
Tumorigenesis
Tumors
Xenografts
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Title Establishing of mouse oral carcinoma cell lines derived from transgenic mice and their use as syngeneic tumorigenesis models
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