Identification of lymphocyte cell-specific protein-tyrosine kinase (LCK) as a driver for invasion and migration of oral cancer by tumor heterogeneity exploitation

Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence, the identification of novel therapeutic targets is an urgent need. However, tumors are comprised of a heterogeneous collection of cells with distinct g...

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Published inMolecular cancer Vol. 20; no. 1; pp. 88 - 23
Main Authors Weiße, Jonas, Rosemann, Julia, Müller, Lisa, Kappler, Matthias, Eckert, Alexander W., Glaß, Markus, Misiak, Danny, Hüttelmaier, Stefan, Ballhausen, Wolfgang G., Hatzfeld, Mechthild, Haemmerle, Monika, Gutschner, Tony
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 11.06.2021
BioMed Central
BMC
Subjects
Adherens junctions
Analysis
Antineoplastic Agents - pharmacology
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - pathology
Cell culture
Cell differentiation
Cell Line, Tumor
Cell Movement - drug effects
Cell Movement - genetics
Clonal heterogeneity
Dasatinib
Dasatinib - pharmacology
EMT
Gene expression
Health aspects
HNSCC
Humans
Invasion
Invasiveness
ITH
Kinases
Lck protein
Lethality
Leukocyte migration
Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - genetics
Lymphocytes
Metastases
Metastasis
Motility
Mouth cancer
Mouth Neoplasms - genetics
Mouth Neoplasms - pathology
Neoplasm Invasiveness - genetics
Neoplasm Invasiveness - pathology
Oral cancer
Phenols
Protein-tyrosine kinase
Proteins
RNA
Scientific equipment and supplies industry
Therapeutic targets
Tongue
Transcriptome
Transcriptomes
Tumor cell lines
Tumors
Tyrosine
United States
New York
United States > US
Dasatinib
OSCC
Src
HNSCC
Clonal heterogeneity
Metastasis
ITH
EMT
Invasion
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Abstract Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence, the identification of novel therapeutic targets is an urgent need. However, tumors are comprised of a heterogeneous collection of cells with distinct genetic and molecular profiles that can differentially promote metastasis making therapy development a challenging task. Here, we leveraged intratumoral heterogeneity in order to identify drivers of cancer cell motility that might be druggable targets for anti-metastasis therapy. We used 2D migration and 3D matrigel-based invasion assays to characterize the invasive heterogeneity among and within four human oral cancer cell lines in vitro. Subsequently, we applied mRNA-sequencing to map the transcriptomes of poorly and strongly invasive subclones as well as primary tumors and matched metastasis. We identified SAS cells as a highly invasive oral cancer cell line. Clonal analysis of SAS yielded a panel of 20 subclones with different invasive capacities. Integrative gene expression analysis identified the Lymphocyte cell-specific protein-tyrosine kinase (LCK) as a druggable target gene associated with cancer cell invasion and metastasis. Inhibition of LCK using A-770041 or dasatinib blocked invasion of highly aggressive SAS cells. Interestingly, reduction of LCK activity increased the formation of adherens junctions and induced cell differentiation. Analysis of invasive heterogeneity led to the discovery of LCK as an important regulator of motility in oral cancer cells. Hence, small molecule mediated inhibition of LCK could be a promising anti-metastasis therapy option for oral cancer patients.
AbstractList Abstract Background Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence, the identification of novel therapeutic targets is an urgent need. However, tumors are comprised of a heterogeneous collection of cells with distinct genetic and molecular profiles that can differentially promote metastasis making therapy development a challenging task. Here, we leveraged intratumoral heterogeneity in order to identify drivers of cancer cell motility that might be druggable targets for anti-metastasis therapy. Methods We used 2D migration and 3D matrigel-based invasion assays to characterize the invasive heterogeneity among and within four human oral cancer cell lines in vitro. Subsequently, we applied mRNA-sequencing to map the transcriptomes of poorly and strongly invasive subclones as well as primary tumors and matched metastasis. Results We identified SAS cells as a highly invasive oral cancer cell line. Clonal analysis of SAS yielded a panel of 20 subclones with different invasive capacities. Integrative gene expression analysis identified the Lymphocyte cell-specific protein-tyrosine kinase (LCK) as a druggable target gene associated with cancer cell invasion and metastasis. Inhibition of LCK using A-770041 or dasatinib blocked invasion of highly aggressive SAS cells. Interestingly, reduction of LCK activity increased the formation of adherens junctions and induced cell differentiation. Conclusion Analysis of invasive heterogeneity led to the discovery of LCK as an important regulator of motility in oral cancer cells. Hence, small molecule mediated inhibition of LCK could be a promising anti-metastasis therapy option for oral cancer patients.
Background Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence, the identification of novel therapeutic targets is an urgent need. However, tumors are comprised of a heterogeneous collection of cells with distinct genetic and molecular profiles that can differentially promote metastasis making therapy development a challenging task. Here, we leveraged intratumoral heterogeneity in order to identify drivers of cancer cell motility that might be druggable targets for anti-metastasis therapy. Methods We used 2D migration and 3D matrigel-based invasion assays to characterize the invasive heterogeneity among and within four human oral cancer cell lines in vitro. Subsequently, we applied mRNA-sequencing to map the transcriptomes of poorly and strongly invasive subclones as well as primary tumors and matched metastasis. Results We identified SAS cells as a highly invasive oral cancer cell line. Clonal analysis of SAS yielded a panel of 20 subclones with different invasive capacities. Integrative gene expression analysis identified the Lymphocyte cell-specific protein-tyrosine kinase (LCK) as a druggable target gene associated with cancer cell invasion and metastasis. Inhibition of LCK using A-770041 or dasatinib blocked invasion of highly aggressive SAS cells. Interestingly, reduction of LCK activity increased the formation of adherens junctions and induced cell differentiation. Conclusion Analysis of invasive heterogeneity led to the discovery of LCK as an important regulator of motility in oral cancer cells. Hence, small molecule mediated inhibition of LCK could be a promising anti-metastasis therapy option for oral cancer patients. Keywords: Clonal heterogeneity, Dasatinib, EMT, HNSCC, Invasion, ITH, Metastasis, OSCC, Src
Background Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence, the identification of novel therapeutic targets is an urgent need. However, tumors are comprised of a heterogeneous collection of cells with distinct genetic and molecular profiles that can differentially promote metastasis making therapy development a challenging task. Here, we leveraged intratumoral heterogeneity in order to identify drivers of cancer cell motility that might be druggable targets for anti-metastasis therapy. Methods We used 2D migration and 3D matrigel-based invasion assays to characterize the invasive heterogeneity among and within four human oral cancer cell lines in vitro. Subsequently, we applied mRNA-sequencing to map the transcriptomes of poorly and strongly invasive subclones as well as primary tumors and matched metastasis. Results We identified SAS cells as a highly invasive oral cancer cell line. Clonal analysis of SAS yielded a panel of 20 subclones with different invasive capacities. Integrative gene expression analysis identified the Lymphocyte cell-specific protein-tyrosine kinase (LCK) as a druggable target gene associated with cancer cell invasion and metastasis. Inhibition of LCK using A-770041 or dasatinib blocked invasion of highly aggressive SAS cells. Interestingly, reduction of LCK activity increased the formation of adherens junctions and induced cell differentiation. Conclusion Analysis of invasive heterogeneity led to the discovery of LCK as an important regulator of motility in oral cancer cells. Hence, small molecule mediated inhibition of LCK could be a promising anti-metastasis therapy option for oral cancer patients.
Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence, the identification of novel therapeutic targets is an urgent need. However, tumors are comprised of a heterogeneous collection of cells with distinct genetic and molecular profiles that can differentially promote metastasis making therapy development a challenging task. Here, we leveraged intratumoral heterogeneity in order to identify drivers of cancer cell motility that might be druggable targets for anti-metastasis therapy.BACKGROUNDCancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence, the identification of novel therapeutic targets is an urgent need. However, tumors are comprised of a heterogeneous collection of cells with distinct genetic and molecular profiles that can differentially promote metastasis making therapy development a challenging task. Here, we leveraged intratumoral heterogeneity in order to identify drivers of cancer cell motility that might be druggable targets for anti-metastasis therapy.We used 2D migration and 3D matrigel-based invasion assays to characterize the invasive heterogeneity among and within four human oral cancer cell lines in vitro. Subsequently, we applied mRNA-sequencing to map the transcriptomes of poorly and strongly invasive subclones as well as primary tumors and matched metastasis.METHODSWe used 2D migration and 3D matrigel-based invasion assays to characterize the invasive heterogeneity among and within four human oral cancer cell lines in vitro. Subsequently, we applied mRNA-sequencing to map the transcriptomes of poorly and strongly invasive subclones as well as primary tumors and matched metastasis.We identified SAS cells as a highly invasive oral cancer cell line. Clonal analysis of SAS yielded a panel of 20 subclones with different invasive capacities. Integrative gene expression analysis identified the Lymphocyte cell-specific protein-tyrosine kinase (LCK) as a druggable target gene associated with cancer cell invasion and metastasis. Inhibition of LCK using A-770041 or dasatinib blocked invasion of highly aggressive SAS cells. Interestingly, reduction of LCK activity increased the formation of adherens junctions and induced cell differentiation.RESULTSWe identified SAS cells as a highly invasive oral cancer cell line. Clonal analysis of SAS yielded a panel of 20 subclones with different invasive capacities. Integrative gene expression analysis identified the Lymphocyte cell-specific protein-tyrosine kinase (LCK) as a druggable target gene associated with cancer cell invasion and metastasis. Inhibition of LCK using A-770041 or dasatinib blocked invasion of highly aggressive SAS cells. Interestingly, reduction of LCK activity increased the formation of adherens junctions and induced cell differentiation.Analysis of invasive heterogeneity led to the discovery of LCK as an important regulator of motility in oral cancer cells. Hence, small molecule mediated inhibition of LCK could be a promising anti-metastasis therapy option for oral cancer patients.CONCLUSIONAnalysis of invasive heterogeneity led to the discovery of LCK as an important regulator of motility in oral cancer cells. Hence, small molecule mediated inhibition of LCK could be a promising anti-metastasis therapy option for oral cancer patients.
Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence, the identification of novel therapeutic targets is an urgent need. However, tumors are comprised of a heterogeneous collection of cells with distinct genetic and molecular profiles that can differentially promote metastasis making therapy development a challenging task. Here, we leveraged intratumoral heterogeneity in order to identify drivers of cancer cell motility that might be druggable targets for anti-metastasis therapy. We used 2D migration and 3D matrigel-based invasion assays to characterize the invasive heterogeneity among and within four human oral cancer cell lines in vitro. Subsequently, we applied mRNA-sequencing to map the transcriptomes of poorly and strongly invasive subclones as well as primary tumors and matched metastasis. We identified SAS cells as a highly invasive oral cancer cell line. Clonal analysis of SAS yielded a panel of 20 subclones with different invasive capacities. Integrative gene expression analysis identified the Lymphocyte cell-specific protein-tyrosine kinase (LCK) as a druggable target gene associated with cancer cell invasion and metastasis. Inhibition of LCK using A-770041 or dasatinib blocked invasion of highly aggressive SAS cells. Interestingly, reduction of LCK activity increased the formation of adherens junctions and induced cell differentiation. Analysis of invasive heterogeneity led to the discovery of LCK as an important regulator of motility in oral cancer cells. Hence, small molecule mediated inhibition of LCK could be a promising anti-metastasis therapy option for oral cancer patients.
Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence, the identification of novel therapeutic targets is an urgent need. However, tumors are comprised of a heterogeneous collection of cells with distinct genetic and molecular profiles that can differentially promote metastasis making therapy development a challenging task. Here, we leveraged intratumoral heterogeneity in order to identify drivers of cancer cell motility that might be druggable targets for anti-metastasis therapy. We used 2D migration and 3D matrigel-based invasion assays to characterize the invasive heterogeneity among and within four human oral cancer cell lines in vitro. Subsequently, we applied mRNA-sequencing to map the transcriptomes of poorly and strongly invasive subclones as well as primary tumors and matched metastasis. We identified SAS cells as a highly invasive oral cancer cell line. Clonal analysis of SAS yielded a panel of 20 subclones with different invasive capacities. Integrative gene expression analysis identified the Lymphocyte cell-specific protein-tyrosine kinase (LCK) as a druggable target gene associated with cancer cell invasion and metastasis. Inhibition of LCK using A-770041 or dasatinib blocked invasion of highly aggressive SAS cells. Interestingly, reduction of LCK activity increased the formation of adherens junctions and induced cell differentiation. Analysis of invasive heterogeneity led to the discovery of LCK as an important regulator of motility in oral cancer cells. Hence, small molecule mediated inhibition of LCK could be a promising anti-metastasis therapy option for oral cancer patients.
ArticleNumber 88
Audience Academic
Author Kappler, Matthias
Ballhausen, Wolfgang G.
Hatzfeld, Mechthild
Eckert, Alexander W.
Weiße, Jonas
Haemmerle, Monika
Hüttelmaier, Stefan
Müller, Lisa
Rosemann, Julia
Misiak, Danny
Gutschner, Tony
Glaß, Markus
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  surname: Gutschner
  fullname: Gutschner, Tony
BackLink https://www.ncbi.nlm.nih.gov/pubmed/34116687$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1016/j.oraloncology.2017.03.011
10.1038/ncomms2928
10.3892/ijo.2016.3788
10.1016/j.oraloncology.2017.02.017
10.3390/ijms20143500
10.1517/14728222.2013.740012
10.1038/s41388-018-0546-z
10.1021/jm049486a
10.1016/j.oraloncology.2019.104551
10.1093/jnci/59.6.1611
10.1038/nmeth.2019
10.1016/j.ccell.2020.06.006
10.1016/j.ccell.2018.12.002
10.1002/cam4.27
10.1158/0008-5472.CAN-19-0458
10.1002/1521-4141(200102)31:2<323::AID-IMMU323>3.0.CO;2-0
10.1158/1535-7163.MCT-10-0096
10.1158/0008-5472.CAN-12-1803
10.2353/ajpath.2006.050570
10.1038/s41586-020-2969-2
10.1007/s10549-018-05100-z
10.18632/oncotarget.15680
10.1158/2159-8290.CD-15-0439
10.1158/1078-0432.CCR-10-0066
10.1016/S1470-2045(13)70479-0
10.1016/j.clbc.2011.03.021
10.1016/j.bmcl.2005.09.039
10.1016/j.ccell.2020.06.012
10.1016/j.neo.2017.05.002
10.1242/dev.139071
10.1038/s41586-019-1186-3
10.1002/cam4.229
10.1111/jop.12306
10.1016/j.oraloncology.2011.12.013
10.1007/s10637-012-9897-4
10.1124/jpet.105.089169
10.1016/j.cell.2011.09.024
10.1093/nar/gkz430
10.1053/j.gastro.2010.03.034
10.1158/1078-0432.CCR-14-0800
10.1126/scisignal.2004088
10.1007/s10549-016-3911-z
10.1093/annonc/mdw014
10.1002/cncr.25769
10.1006/geno.1996.0364
10.3389/fonc.2020.00747
10.1186/s13045-017-0418-y
10.1097/00005537-200010000-00038
10.1093/annonc/mdw607
10.1172/JCI74440
10.1007/BF01209653
10.3892/ijo.3.2.369
10.1158/1078-0432.CCR-11-3359
10.1056/NEJMp1607591
10.1186/s12916-017-0900-y
10.1002/cncr.30663
10.1111/cas.13522
10.1016/0092-8674(92)90428-F
10.3322/caac.21492
10.4103/0971-5851.96966
10.1016/j.jcms.2014.11.007
10.1016/j.devcel.2019.04.010
10.3389/fimmu.2019.00208
10.5125/jkaoms.2019.45.2.83
10.1002/ijc.1461
10.1002/pros.23119
10.1371/journal.pone.0077099
10.1242/jcs.238295
10.1158/1078-0432.CCR-11-1071
10.1007/s00404-020-05496-4
10.1634/theoncologist.2013-0255
10.1038/nrclinonc.2014.192
10.1038/s41419-019-1769-9
10.4103/jomfp.JOMFP_334_19
10.3390/cells8101118
10.1074/jbc.M311400200
10.1007/s10637-011-9650-4
10.1002/hed.24687
10.1093/carcin/bgt021
10.1038/s41568-019-0213-x
10.1016/j.oraloncology.2008.05.015
10.1158/2159-8290.CD-12-0095
10.1186/s12943-018-0937-3
10.1093/jrr/rrz003
10.1111/j.0022-202X.2004.23530.x
10.1016/j.jbo.2019.100261
10.1016/0003-2697(87)90021-2
10.1016/j.ccr.2014.03.020
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Issue 1
Keywords Dasatinib
OSCC
Src
HNSCC
Clonal heterogeneity
Metastasis
ITH
EMT
Invasion
Language English
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References G Sokeland (1384_CR37) 2019; 18
ED Williams (1384_CR21) 2019; 19
CI Herold (1384_CR78) 2011; 17
W Lu (1384_CR19) 2019; 49
D Adams (1384_CR61) 1976; 58
N Harashima (1384_CR56) 2001; 31
MH Chien (1384_CR36) 2013; 17
TC Gangadhar (1384_CR76) 2013; 31
J Gao (1384_CR34) 2013; 6
L Chen (1384_CR41) 2017; 50
S Groeger (1384_CR3) 2019; 10
DB Gissi (1384_CR23) 2017; 67
K Mayer (1384_CR57) 1993; 3
N Imai (1384_CR89) 2001; 94
K Campbell (1384_CR20) 2016; 143
P Chomczynski (1384_CR26) 1987; 162
1384_CR28
S Matsueda (1384_CR90) 2018; 109
HD Brooks (1384_CR87) 2011; 117
DR Caswell (1384_CR55) 2017; 15
JC Araujo (1384_CR71) 2013; 14
XM Zhang (1384_CR45) 2019; 60
LP Stabile (1384_CR88) 2017; 69
PK Ha (1384_CR25) 2009; 45
DS Chandrashekar (1384_CR31) 2017; 19
Z Tang (1384_CR32) 2019; 47
X Li (1384_CR59) 2014; 25
JG Trevino (1384_CR69) 2006; 168
L Pusztai (1384_CR84) 2014; 20
LJ Lombardo (1384_CR54) 2004; 47
TRJ Evans (1384_CR75) 2017; 28
W van Roosmalen (1384_CR49) 2015; 125
J Arcaroli (1384_CR72) 2012; 1
JP Morton (1384_CR68) 2010; 139
A Ocana (1384_CR81) 2019; 174
T Powles (1384_CR83) 2016; 27
K Okumura (1384_CR39) 1996; 122
E Cerami (1384_CR33) 2012; 2
CM Chan (1384_CR65) 2012; 18
A Gucalp (1384_CR77) 2011; 11
A Miranda-Filho (1384_CR2) 2020; 102
YC Sim (1384_CR12) 2019; 45
D Ishay-Ronen (1384_CR63) 2019; 35
JJ Arcaroli (1384_CR64) 2010; 16
S Graham (1384_CR7) 1977; 59
RL Grossman (1384_CR35) 2016; 375
XH Tang (1384_CR4) 2013; 34
E Alsahafi (1384_CR9) 2019; 10
A Burchat (1384_CR52) 2006; 16
F Bray (1384_CR1) 2018; 68
WA Schroder (1384_CR44) 2014; 3
MA Rogers (1384_CR62) 2005; 124
MG Fury (1384_CR86) 2011; 31
S Zhang (1384_CR70) 2013; 73
EM Posadas (1384_CR82) 2016; 76
DB Straus (1384_CR58) 1992; 70
GH Mahabeleshwar (1384_CR47) 2004; 279
K Kalinsky (1384_CR79) 2017; 123
M Ghandi (1384_CR29) 2019; 569
SS Muttagi (1384_CR8) 2012; 33
HJ Mackay (1384_CR80) 2012; 30
L Morandi (1384_CR24) 2015; 43
S Danson (1384_CR74) 2019; 19
JK Ness (1384_CR51) 2013; 4
J Schindelin (1384_CR27) 2012; 9
LM LaFave (1384_CR15) 2020; 38
1384_CR46
S Valastyan (1384_CR14) 2011; 147
M Greaves (1384_CR22) 2015; 5
H Kang (1384_CR10) 2015; 12
M de Camargo Cancela (1384_CR6) 2012; 48
DG Sessions (1384_CR11) 2000; 110
AM Lopez-Colome (1384_CR60) 2017; 10
F Duprez (1384_CR13) 2017; 39
X Jin (1384_CR30) 2020; 588
JM Levitt (1384_CR67) 2010; 9
K Nakahira (1384_CR48) 2013; 8
DR Welch (1384_CR17) 2019; 79
T Heilmann (1384_CR66) 2020; 301
N Vig (1384_CR5) 2015; 44
P Jayanthi (1384_CR18) 2020; 24
RF Stachlewitz (1384_CR53) 2005; 315
A Berberich (1384_CR42) 2020; 10
JP Zepecki (1384_CR50) 2019; 38
ND Marjanovic (1384_CR16) 2020; 38
1384_CR38
T Jin (1384_CR43) 2017; 8
AF Schott (1384_CR85) 2016; 159
CE Chee (1384_CR73) 2013; 18
CN Adra (1384_CR40) 1996; 35
36918841 - Mol Cancer. 2023 Mar 14;22(1):50
References_xml – volume: 69
  start-page: 38
  year: 2017
  ident: 1384_CR88
  publication-title: Oral Oncol
  doi: 10.1016/j.oraloncology.2017.03.011
– volume: 4
  start-page: 1912
  issue: 1
  year: 2013
  ident: 1384_CR51
  publication-title: Nat Commun
  doi: 10.1038/ncomms2928
– volume: 50
  start-page: 263
  issue: 1
  year: 2017
  ident: 1384_CR41
  publication-title: Int J Oncol
  doi: 10.3892/ijo.2016.3788
– volume: 67
  start-page: 131
  year: 2017
  ident: 1384_CR23
  publication-title: Oral Oncol
  doi: 10.1016/j.oraloncology.2017.02.017
– ident: 1384_CR46
  doi: 10.3390/ijms20143500
– volume: 31
  start-page: 249
  issue: 1
  year: 2011
  ident: 1384_CR86
  publication-title: Anticancer Res
– volume: 17
  start-page: 203
  issue: 2
  year: 2013
  ident: 1384_CR36
  publication-title: Expert Opin Ther Targets
  doi: 10.1517/14728222.2013.740012
– volume: 38
  start-page: 1734
  issue: 10
  year: 2019
  ident: 1384_CR50
  publication-title: Oncogene
  doi: 10.1038/s41388-018-0546-z
– volume: 47
  start-page: 6658
  issue: 27
  year: 2004
  ident: 1384_CR54
  publication-title: J Med Chem
  doi: 10.1021/jm049486a
– volume: 102
  start-page: 104551
  year: 2020
  ident: 1384_CR2
  publication-title: Oral Oncol
  doi: 10.1016/j.oraloncology.2019.104551
– volume: 59
  start-page: 1611
  issue: 6
  year: 1977
  ident: 1384_CR7
  publication-title: J Natl Cancer Inst
  doi: 10.1093/jnci/59.6.1611
– volume: 9
  start-page: 676
  issue: 7
  year: 2012
  ident: 1384_CR27
  publication-title: Nat Methods
  doi: 10.1038/nmeth.2019
– volume: 38
  start-page: 212
  issue: 2
  year: 2020
  ident: 1384_CR15
  publication-title: Cancer Cell
  doi: 10.1016/j.ccell.2020.06.006
– volume: 35
  start-page: 17
  issue: 1
  year: 2019
  ident: 1384_CR63
  publication-title: Cancer Cell
  doi: 10.1016/j.ccell.2018.12.002
– volume: 1
  start-page: 207
  issue: 2
  year: 2012
  ident: 1384_CR72
  publication-title: Cancer Med
  doi: 10.1002/cam4.27
– volume: 79
  start-page: 3011
  issue: 12
  year: 2019
  ident: 1384_CR17
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-19-0458
– volume: 31
  start-page: 323
  issue: 2
  year: 2001
  ident: 1384_CR56
  publication-title: Eur J Immunol
  doi: 10.1002/1521-4141(200102)31:2<323::AID-IMMU323>3.0.CO;2-0
– volume: 9
  start-page: 1128
  issue: 5
  year: 2010
  ident: 1384_CR67
  publication-title: Mol Cancer Ther
  doi: 10.1158/1535-7163.MCT-10-0096
– volume: 73
  start-page: 5764
  issue: 18
  year: 2013
  ident: 1384_CR70
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-12-1803
– volume: 168
  start-page: 962
  issue: 3
  year: 2006
  ident: 1384_CR69
  publication-title: Am J Pathol
  doi: 10.2353/ajpath.2006.050570
– volume: 588
  start-page: 331
  issue: 7837
  year: 2020
  ident: 1384_CR30
  publication-title: Nature
  doi: 10.1038/s41586-020-2969-2
– volume: 174
  start-page: 693
  issue: 3
  year: 2019
  ident: 1384_CR81
  publication-title: Breast Cancer Res Treat
  doi: 10.1007/s10549-018-05100-z
– volume: 8
  start-page: 32769
  issue: 20
  year: 2017
  ident: 1384_CR43
  publication-title: Oncotarget
  doi: 10.18632/oncotarget.15680
– volume: 5
  start-page: 806
  issue: 8
  year: 2015
  ident: 1384_CR22
  publication-title: Cancer Discov
  doi: 10.1158/2159-8290.CD-15-0439
– volume: 16
  start-page: 4165
  issue: 16
  year: 2010
  ident: 1384_CR64
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-10-0066
– volume: 14
  start-page: 1307
  issue: 13
  year: 2013
  ident: 1384_CR71
  publication-title: Lancet Oncol
  doi: 10.1016/S1470-2045(13)70479-0
– volume: 11
  start-page: 306
  issue: 5
  year: 2011
  ident: 1384_CR77
  publication-title: Clin Breast Cancer
  doi: 10.1016/j.clbc.2011.03.021
– volume: 16
  start-page: 118
  issue: 1
  year: 2006
  ident: 1384_CR52
  publication-title: Bioorg Med Chem Lett
  doi: 10.1016/j.bmcl.2005.09.039
– volume: 38
  start-page: 229
  issue: 2
  year: 2020
  ident: 1384_CR16
  publication-title: Cancer Cell
  doi: 10.1016/j.ccell.2020.06.012
– volume: 19
  start-page: 649
  issue: 8
  year: 2017
  ident: 1384_CR31
  publication-title: Neoplasia
  doi: 10.1016/j.neo.2017.05.002
– volume: 143
  start-page: 4291
  issue: 23
  year: 2016
  ident: 1384_CR20
  publication-title: Development
  doi: 10.1242/dev.139071
– volume: 569
  start-page: 503
  issue: 7757
  year: 2019
  ident: 1384_CR29
  publication-title: Nature
  doi: 10.1038/s41586-019-1186-3
– volume: 3
  start-page: 500
  issue: 3
  year: 2014
  ident: 1384_CR44
  publication-title: Cancer Med
  doi: 10.1002/cam4.229
– volume: 44
  start-page: 649
  issue: 9
  year: 2015
  ident: 1384_CR5
  publication-title: J Oral Pathol Med
  doi: 10.1111/jop.12306
– volume: 48
  start-page: 484
  issue: 6
  year: 2012
  ident: 1384_CR6
  publication-title: Oral Oncol
  doi: 10.1016/j.oraloncology.2011.12.013
– volume: 31
  start-page: 769
  issue: 3
  year: 2013
  ident: 1384_CR76
  publication-title: Investig New Drugs
  doi: 10.1007/s10637-012-9897-4
– volume: 315
  start-page: 36
  issue: 1
  year: 2005
  ident: 1384_CR53
  publication-title: J Pharmacol Exp Ther
  doi: 10.1124/jpet.105.089169
– volume: 147
  start-page: 275
  issue: 2
  year: 2011
  ident: 1384_CR14
  publication-title: Cell
  doi: 10.1016/j.cell.2011.09.024
– volume: 47
  start-page: W556
  issue: W1
  year: 2019
  ident: 1384_CR32
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gkz430
– volume: 139
  start-page: 292
  issue: 1
  year: 2010
  ident: 1384_CR68
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2010.03.034
– volume: 20
  start-page: 5265
  issue: 20
  year: 2014
  ident: 1384_CR84
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-14-0800
– volume: 6
  start-page: pl1
  issue: 269
  year: 2013
  ident: 1384_CR34
  publication-title: Sci Signal
  doi: 10.1126/scisignal.2004088
– volume: 159
  start-page: 87
  issue: 1
  year: 2016
  ident: 1384_CR85
  publication-title: Breast Cancer Res Treat
  doi: 10.1007/s10549-016-3911-z
– volume: 27
  start-page: 880
  issue: 5
  year: 2016
  ident: 1384_CR83
  publication-title: Ann Oncol
  doi: 10.1093/annonc/mdw014
– volume: 117
  start-page: 2112
  issue: 10
  year: 2011
  ident: 1384_CR87
  publication-title: Cancer
  doi: 10.1002/cncr.25769
– volume: 35
  start-page: 328
  issue: 2
  year: 1996
  ident: 1384_CR40
  publication-title: Genomics
  doi: 10.1006/geno.1996.0364
– volume: 10
  start-page: 747
  year: 2020
  ident: 1384_CR42
  publication-title: Front Oncol
  doi: 10.3389/fonc.2020.00747
– volume: 10
  start-page: 50
  issue: 1
  year: 2017
  ident: 1384_CR60
  publication-title: J Hematol Oncol
  doi: 10.1186/s13045-017-0418-y
– volume: 110
  start-page: 1764
  issue: 10 Pt 1
  year: 2000
  ident: 1384_CR11
  publication-title: Laryngoscope
  doi: 10.1097/00005537-200010000-00038
– volume: 28
  start-page: 354
  issue: 2
  year: 2017
  ident: 1384_CR75
  publication-title: Ann Oncol
  doi: 10.1093/annonc/mdw607
– volume: 125
  start-page: 1648
  issue: 4
  year: 2015
  ident: 1384_CR49
  publication-title: J Clin Invest
  doi: 10.1172/JCI74440
– volume: 122
  start-page: 243
  issue: 4
  year: 1996
  ident: 1384_CR39
  publication-title: J Cancer Res Clin Oncol
  doi: 10.1007/BF01209653
– volume: 3
  start-page: 369
  issue: 2
  year: 1993
  ident: 1384_CR57
  publication-title: Int J Oncol
  doi: 10.3892/ijo.3.2.369
– volume: 18
  start-page: 3580
  issue: 13
  year: 2012
  ident: 1384_CR65
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-11-3359
– volume: 375
  start-page: 1109
  issue: 12
  year: 2016
  ident: 1384_CR35
  publication-title: N Engl J Med
  doi: 10.1056/NEJMp1607591
– volume: 15
  start-page: 133
  issue: 1
  year: 2017
  ident: 1384_CR55
  publication-title: BMC Med
  doi: 10.1186/s12916-017-0900-y
– volume: 58
  start-page: 351
  issue: 5
  year: 1976
  ident: 1384_CR61
  publication-title: Ann R Coll Surg Engl
– volume: 123
  start-page: 2688
  issue: 14
  year: 2017
  ident: 1384_CR79
  publication-title: Cancer
  doi: 10.1002/cncr.30663
– volume: 109
  start-page: 611
  issue: 3
  year: 2018
  ident: 1384_CR90
  publication-title: Cancer Sci
  doi: 10.1111/cas.13522
– volume: 70
  start-page: 585
  issue: 4
  year: 1992
  ident: 1384_CR58
  publication-title: Cell
  doi: 10.1016/0092-8674(92)90428-F
– volume: 68
  start-page: 394
  issue: 6
  year: 2018
  ident: 1384_CR1
  publication-title: CA Cancer J Clin
  doi: 10.3322/caac.21492
– volume: 33
  start-page: 32
  issue: 1
  year: 2012
  ident: 1384_CR8
  publication-title: Indian J Med Paediatr Oncol
  doi: 10.4103/0971-5851.96966
– volume: 43
  start-page: 208
  issue: 2
  year: 2015
  ident: 1384_CR24
  publication-title: J Craniomaxillofac Surg
  doi: 10.1016/j.jcms.2014.11.007
– volume: 49
  start-page: 361
  issue: 3
  year: 2019
  ident: 1384_CR19
  publication-title: Dev Cell
  doi: 10.1016/j.devcel.2019.04.010
– volume: 10
  start-page: 208
  year: 2019
  ident: 1384_CR3
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2019.00208
– volume: 45
  start-page: 83
  issue: 2
  year: 2019
  ident: 1384_CR12
  publication-title: J Korean Assoc Oral Maxillofac Surg
  doi: 10.5125/jkaoms.2019.45.2.83
– volume: 94
  start-page: 237
  issue: 2
  year: 2001
  ident: 1384_CR89
  publication-title: Int J Cancer
  doi: 10.1002/ijc.1461
– volume: 76
  start-page: 286
  issue: 3
  year: 2016
  ident: 1384_CR82
  publication-title: Prostate
  doi: 10.1002/pros.23119
– volume: 8
  issue: 10
  year: 2013
  ident: 1384_CR48
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0077099
– ident: 1384_CR28
  doi: 10.1242/jcs.238295
– volume: 17
  start-page: 6061
  issue: 18
  year: 2011
  ident: 1384_CR78
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-11-1071
– volume: 301
  start-page: 1493
  issue: 6
  year: 2020
  ident: 1384_CR66
  publication-title: Arch Gynecol Obstet
  doi: 10.1007/s00404-020-05496-4
– volume: 18
  start-page: 1091
  issue: 10
  year: 2013
  ident: 1384_CR73
  publication-title: Oncologist
  doi: 10.1634/theoncologist.2013-0255
– volume: 12
  start-page: 11
  issue: 1
  year: 2015
  ident: 1384_CR10
  publication-title: Nat Rev Clin Oncol
  doi: 10.1038/nrclinonc.2014.192
– volume: 10
  start-page: 540
  issue: 8
  year: 2019
  ident: 1384_CR9
  publication-title: Cell Death Dis
  doi: 10.1038/s41419-019-1769-9
– volume: 24
  start-page: 189
  issue: 1
  year: 2020
  ident: 1384_CR18
  publication-title: J Oral Maxillofac Pathol
  doi: 10.4103/jomfp.JOMFP_334_19
– ident: 1384_CR38
  doi: 10.3390/cells8101118
– volume: 279
  start-page: 9733
  issue: 11
  year: 2004
  ident: 1384_CR47
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M311400200
– volume: 30
  start-page: 1158
  issue: 3
  year: 2012
  ident: 1384_CR80
  publication-title: Investig New Drugs
  doi: 10.1007/s10637-011-9650-4
– volume: 39
  start-page: 1733
  issue: 9
  year: 2017
  ident: 1384_CR13
  publication-title: Head Neck
  doi: 10.1002/hed.24687
– volume: 34
  start-page: 1158
  issue: 5
  year: 2013
  ident: 1384_CR4
  publication-title: Carcinogenesis
  doi: 10.1093/carcin/bgt021
– volume: 19
  start-page: 716
  issue: 12
  year: 2019
  ident: 1384_CR21
  publication-title: Nat Rev Cancer
  doi: 10.1038/s41568-019-0213-x
– volume: 45
  start-page: 335
  issue: 4–5
  year: 2009
  ident: 1384_CR25
  publication-title: Oral Oncol
  doi: 10.1016/j.oraloncology.2008.05.015
– volume: 2
  start-page: 401
  issue: 5
  year: 2012
  ident: 1384_CR33
  publication-title: Cancer Discov
  doi: 10.1158/2159-8290.CD-12-0095
– volume: 18
  start-page: 12
  issue: 1
  year: 2019
  ident: 1384_CR37
  publication-title: Mol Cancer
  doi: 10.1186/s12943-018-0937-3
– volume: 60
  start-page: 318
  issue: 3
  year: 2019
  ident: 1384_CR45
  publication-title: J Radiat Res
  doi: 10.1093/jrr/rrz003
– volume: 124
  start-page: 536
  issue: 3
  year: 2005
  ident: 1384_CR62
  publication-title: J Invest Dermatol
  doi: 10.1111/j.0022-202X.2004.23530.x
– volume: 19
  start-page: 100261
  year: 2019
  ident: 1384_CR74
  publication-title: J Bone Oncol
  doi: 10.1016/j.jbo.2019.100261
– volume: 162
  start-page: 156
  issue: 1
  year: 1987
  ident: 1384_CR26
  publication-title: Anal Biochem
  doi: 10.1016/0003-2697(87)90021-2
– volume: 25
  start-page: 575
  issue: 5
  year: 2014
  ident: 1384_CR59
  publication-title: Cancer Cell
  doi: 10.1016/j.ccr.2014.03.020
– reference: 36918841 - Mol Cancer. 2023 Mar 14;22(1):50
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Snippet Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence, the...
Background Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is 30%. Hence,...
Abstract Background Cancer metastases are the main cause of lethality. The five-year survival rate for patients diagnosed with advanced stage oral cancer is...
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StartPage 88
SubjectTerms Adherens junctions
Analysis
Antineoplastic Agents - pharmacology
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - pathology
Cell culture
Cell differentiation
Cell Line, Tumor
Cell Movement - drug effects
Cell Movement - genetics
Clonal heterogeneity
Dasatinib
Dasatinib - pharmacology
EMT
Gene expression
Health aspects
HNSCC
Humans
Invasion
Invasiveness
ITH
Kinases
Lck protein
Lethality
Leukocyte migration
Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - genetics
Lymphocytes
Metastases
Metastasis
Motility
Mouth cancer
Mouth Neoplasms - genetics
Mouth Neoplasms - pathology
Neoplasm Invasiveness - genetics
Neoplasm Invasiveness - pathology
Oral cancer
Phenols
Protein-tyrosine kinase
Proteins
RNA
Scientific equipment and supplies industry
Therapeutic targets
Tongue
Transcriptome
Transcriptomes
Tumor cell lines
Tumors
Tyrosine
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Title Identification of lymphocyte cell-specific protein-tyrosine kinase (LCK) as a driver for invasion and migration of oral cancer by tumor heterogeneity exploitation
URI https://www.ncbi.nlm.nih.gov/pubmed/34116687
https://www.proquest.com/docview/2543480270
https://www.proquest.com/docview/2540514333
https://pubmed.ncbi.nlm.nih.gov/PMC8194179
https://doaj.org/article/2fab5abc84ca4a3daabdfded742fbe0b
Volume 20
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