Academic Journal

High-Resolution aCGH Analysis of the Jurkat Cell Line: Copy Number Alterations and Their Association With Cancer Hallmarks.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: High-Resolution aCGH Analysis of the Jurkat Cell Line: Copy Number Alterations and Their Association With Cancer Hallmarks.
Συγγραφείς: DA Costa LM; Department of Biological Sciences, Oncology Research Center, Federal University of Pará, Belém, Brazil., Ferreira WAS; Laboratory of Cytogenomics and Environmental Mutagenesis, Environment Section (SAMAM), Evandro Chagas Institute (IEC), Ananindeua, Brazil., Machado CB; Department of Medicine, Clinical Genetics Laboratory, Drug Research and Development Center (NPDM), Federal University of Ceará, Fortaleza, Brazil., Amorim CKN; Laboratory of Cytogenomics and Environmental Mutagenesis, Environment Section (SAMAM), Evandro Chagas Institute (IEC), Ananindeua, Brazil., VAN DEN Berg AV; Department of Medicine, Institute of Medical Sciences, Federal University of Pará, Belém, Brazil., DE Moraes Filho MO; Department of Medicine, Clinical Genetics Laboratory, Drug Research and Development Center (NPDM), Federal University of Ceará, Fortaleza, Brazil., DE Moraes MEA; Department of Medicine, Clinical Genetics Laboratory, Drug Research and Development Center (NPDM), Federal University of Ceará, Fortaleza, Brazil., DE Souza LEB; Regional Blood Center of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil., Khayat AS; Department of Biological Sciences, Oncology Research Center, Federal University of Pará, Belém, Brazil., DE Oliveira EHC; Laboratory of Cytogenomics and Environmental Mutagenesis, Environment Section (SAMAM), Evandro Chagas Institute (IEC), Ananindeua, Brazil., Moreira-Nunes CA; Department of Biological Sciences, Oncology Research Center, Federal University of Pará, Belém, Brazil; carolfam@gmail.com.; Department of Medicine, Clinical Genetics Laboratory, Drug Research and Development Center (NPDM), Federal University of Ceará, Fortaleza, Brazil.; Clementino Fraga Group, Central Unity, Molecular Biology Laboratory, Fortaleza, Brazil.
Πηγή: Cancer genomics & proteomics [Cancer Genomics Proteomics] 2025 Sep-Oct; Vol. 22 (5), pp. 824-835.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: International Institute of Anticancer Research Country of Publication: Greece NLM ID: 101188791 Publication Model: Print Cited Medium: Internet ISSN: 1790-6245 (Electronic) Linking ISSN: 11096535 NLM ISO Abbreviation: Cancer Genomics Proteomics Subsets: MEDLINE
Imprint Name(s): Original Publication: Kapandriti, Attiki, Greece : International Institute of Anticancer Research, [2004]-
Ιατρικοί όροι (MeSH): Comparative Genomic Hybridization*/methods , Precursor T-Cell Lymphoblastic Leukemia-Lymphoma*/genetics , Precursor T-Cell Lymphoblastic Leukemia-Lymphoma*/pathology , DNA Copy Number Variations*, Humans ; Jurkat Cells
Περίληψη: Background/aim: Cell lines serve as valuable in vitro models to study altered cellular signaling pathways, to identify mutations in key oncogenic genes, and to test potential antitumor drugs. The Jurkat cell line, for example, has provided important information about various signaling pathways in lymphoblastic leukemia, establishing most of what is currently known about T-cell receptor (TCR) signaling. However, many aspects of the genome modification of this cell line have not yet been analyzed. To identify genes of potential biological and clinical relevance in acute T-lymphoblastic leukemia (T-ALL), we performed an array comparative genomic hybridization (aCGH) approach on the widely used Jurkat cell line and examined the association of the detected copy number alterations (CNAs) with cancer hallmarks and T-ALL pathogenesis.
Materials and Methods: Cells were harvested by using trypsin/EDTA from culture flasks to extract genomic DNA. aCGH experiments were performed on an Agilent microarray platform using the SurePrint G3 Cancer CGH + SNP Microarray 4×180 K. Functional enrichment analysis of all CNAs was performed with the R package g:Profiler2. The association of these alterations with key cancer hallmarks was analyzed using the Cancer Hallmarks web-tool.
Results: Our analysis revealed several novel CNAs, including losses at 5p15.2, 6q27, 10q22.2, 14q11.2, 18q11.2-q12.1, and Xp22.33, as well as gains at 2p11.2, 7p21.2, 7q21.2 and 18p11.32. Genes within these regions were associated with important oncogenic pathways, including 'sustained proliferative signaling', 'tumor suppressor evasion', and 'angiogenesis promotion'.
Conclusion: These findings suggest that Jurkat cells may serve as a valuable model for identifying new targets for cancer research. Further studies are required to confirm the phenotypic implications of these variants, which may open new avenues for exploring the functional impact of these alterations and their potential role in the development of therapies.
(Copyright © 2025, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)
References: Nucleic Acids Res. 2018 Jan 4;46(D1):D1144-D1149. (PMID: 29099951)
J Clin Invest. 2012 Oct;122(10):3398-406. (PMID: 23023710)
Cancers (Basel). 2020 Jul 20;12(7):. (PMID: 32698360)
Nat Rev Immunol. 2004 Apr;4(4):301-8. (PMID: 15057788)
Exp Mol Med. 2019 Jan 11;51(1):1-15. (PMID: 30635552)
BioData Min. 2013 Oct 16;6(1):18. (PMID: 24131735)
Anticancer Res. 2019 Dec;39(12):6443-6455. (PMID: 31810908)
Nature. 2017 Jun 15;546(7658):426-430. (PMID: 28607489)
Exp Cell Res. 1987 Aug;171(2):389-403. (PMID: 3476309)
Nucleic Acids Res. 2021 Jan 8;49(D1):D1289-D1301. (PMID: 33179738)
Am J Respir Crit Care Med. 2019 Oct 1;200(7):888-899. (PMID: 31166114)
ACS Omega. 2020 Oct 14;5(42):27480-27491. (PMID: 33134711)
J Hematol Oncol. 2016 Oct 24;9(1):114. (PMID: 27776559)
Lancet. 2020 Apr 4;395(10230):1146-1162. (PMID: 32247396)
Mol Cancer Res. 2016 Jan;14(1):3-13. (PMID: 26248648)
Nature. 2019 May;569(7757):503-508. (PMID: 31068700)
Cell Rep. 2018 Apr 3;23(1):227-238.e3. (PMID: 29617662)
F1000Res. 2020 Jul 15;9:. (PMID: 33564394)
Leukemia. 2023 Mar;37(3):529-538. (PMID: 36550215)
Cancers (Basel). 2019 Dec 05;11(12):. (PMID: 31817502)
Nat Rev Clin Oncol. 2013 Mar;10(3):143-53. (PMID: 23400000)
Cancers (Basel). 2020 Jan 03;12(1):. (PMID: 31947841)
Mol Biol Rep. 2020 Jun;47(6):4587-4629. (PMID: 32333246)
Cancers (Basel). 2018 Apr 07;10(4):. (PMID: 29642462)
Cancers (Basel). 2019 Aug 01;11(8):. (PMID: 31374935)
Int J Cancer. 2020 Dec 1;147(11):2988-2995. (PMID: 32406095)
Oncotarget. 2015 Apr 30;6(12):10175-94. (PMID: 25868388)
Anticancer Res. 2019 Sep;39(9):4743-4748. (PMID: 31519574)
J Pharm Anal. 2025 May;15(5):101065. (PMID: 40496069)
J Mater Chem B. 2017 Jun 7;5(21):3970-3981. (PMID: 32264258)
Int J Cancer. 1977 May 15;19(5):621-6. (PMID: 68013)
BMC Genomics. 2018 May 8;19(1):334. (PMID: 29739316)
Genes (Basel). 2021 Jul 23;12(8):. (PMID: 34440292)
Cancer Res. 2019 Nov 15;79(22):5734-5745. (PMID: 31391186)
Contributed Indexing: Keywords: Acute lymphoblastic leukemia; array-based comparative genomic hybridization; tumor cell line
Entry Date(s): Date Created: 20250829 Date Completed: 20250829 Latest Revision: 20250904
Update Code: 20260130
PubMed Central ID: PMC12402711
DOI: 10.21873/cgp.20539
PMID: 40883026
Βάση Δεδομένων: MEDLINE
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  Data: High-Resolution aCGH Analysis of the Jurkat Cell Line: Copy Number Alterations and Their Association With Cancer Hallmarks.
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  Data: <searchLink fieldCode="AU" term="%22DA+Costa+LM%22">DA Costa LM</searchLink>; Department of Biological Sciences, Oncology Research Center, Federal University of Pará, Belém, Brazil.<br /><searchLink fieldCode="AU" term="%22Ferreira+WAS%22">Ferreira WAS</searchLink>; Laboratory of Cytogenomics and Environmental Mutagenesis, Environment Section (SAMAM), Evandro Chagas Institute (IEC), Ananindeua, Brazil.<br /><searchLink fieldCode="AU" term="%22Machado+CB%22">Machado CB</searchLink>; Department of Medicine, Clinical Genetics Laboratory, Drug Research and Development Center (NPDM), Federal University of Ceará, Fortaleza, Brazil.<br /><searchLink fieldCode="AU" term="%22Amorim+CKN%22">Amorim CKN</searchLink>; Laboratory of Cytogenomics and Environmental Mutagenesis, Environment Section (SAMAM), Evandro Chagas Institute (IEC), Ananindeua, Brazil.<br /><searchLink fieldCode="AU" term="%22VAN+DEN+Berg+AV%22">VAN DEN Berg AV</searchLink>; Department of Medicine, Institute of Medical Sciences, Federal University of Pará, Belém, Brazil.<br /><searchLink fieldCode="AU" term="%22DE+Moraes+Filho+MO%22">DE Moraes Filho MO</searchLink>; Department of Medicine, Clinical Genetics Laboratory, Drug Research and Development Center (NPDM), Federal University of Ceará, Fortaleza, Brazil.<br /><searchLink fieldCode="AU" term="%22DE+Moraes+MEA%22">DE Moraes MEA</searchLink>; Department of Medicine, Clinical Genetics Laboratory, Drug Research and Development Center (NPDM), Federal University of Ceará, Fortaleza, Brazil.<br /><searchLink fieldCode="AU" term="%22DE+Souza+LEB%22">DE Souza LEB</searchLink>; Regional Blood Center of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.<br /><searchLink fieldCode="AU" term="%22Khayat+AS%22">Khayat AS</searchLink>; Department of Biological Sciences, Oncology Research Center, Federal University of Pará, Belém, Brazil.<br /><searchLink fieldCode="AU" term="%22DE+Oliveira+EHC%22">DE Oliveira EHC</searchLink>; Laboratory of Cytogenomics and Environmental Mutagenesis, Environment Section (SAMAM), Evandro Chagas Institute (IEC), Ananindeua, Brazil.<br /><searchLink fieldCode="AU" term="%22Moreira-Nunes+CA%22">Moreira-Nunes CA</searchLink>; Department of Biological Sciences, Oncology Research Center, Federal University of Pará, Belém, Brazil; carolfam@gmail.com.; Department of Medicine, Clinical Genetics Laboratory, Drug Research and Development Center (NPDM), Federal University of Ceará, Fortaleza, Brazil.; Clementino Fraga Group, Central Unity, Molecular Biology Laboratory, Fortaleza, Brazil.
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  Data: <i>Publisher: </i><searchLink fieldCode="PB" term="%22International+Institute+of+Anticancer+Research%22">International Institute of Anticancer Research </searchLink><i>Country of Publication: </i>Greece <i>NLM ID: </i>101188791 <i>Publication Model: </i>Print <i>Cited Medium: </i>Internet <i>ISSN: </i>1790-6245 (Electronic) <i>Linking ISSN: </i><searchLink fieldCode="IS" term="%2211096535%22">11096535 </searchLink><i>NLM ISO Abbreviation: </i>Cancer Genomics Proteomics <i>Subsets: </i>MEDLINE
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  Data: <i>Original Publication</i>: Kapandriti, Attiki, Greece : International Institute of Anticancer Research, [2004]-
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  Data: <searchLink fieldCode="MM" term="%22Comparative+Genomic+Hybridization%22">Comparative Genomic Hybridization*</searchLink>/<searchLink fieldCode="MM" term="%22Comparative+Genomic+Hybridization+methods%22">methods</searchLink> <br /><searchLink fieldCode="MM" term="%22Precursor+T-Cell+Lymphoblastic+Leukemia-Lymphoma%22">Precursor T-Cell Lymphoblastic Leukemia-Lymphoma*</searchLink>/<searchLink fieldCode="MM" term="%22Precursor+T-Cell+Lymphoblastic+Leukemia-Lymphoma+genetics%22">genetics</searchLink> <br /><searchLink fieldCode="MM" term="%22Precursor+T-Cell+Lymphoblastic+Leukemia-Lymphoma%22">Precursor T-Cell Lymphoblastic Leukemia-Lymphoma*</searchLink>/<searchLink fieldCode="MM" term="%22Precursor+T-Cell+Lymphoblastic+Leukemia-Lymphoma+pathology%22">pathology</searchLink> <br /><searchLink fieldCode="MM" term="%22DNA+Copy+Number+Variations%22">DNA Copy Number Variations*</searchLink><br /><searchLink fieldCode="MH" term="%22Humans%22">Humans</searchLink> ; <searchLink fieldCode="MH" term="%22Jurkat+Cells%22">Jurkat Cells</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Background/aim: Cell lines serve as valuable in vitro models to study altered cellular signaling pathways, to identify mutations in key oncogenic genes, and to test potential antitumor drugs. The Jurkat cell line, for example, has provided important information about various signaling pathways in lymphoblastic leukemia, establishing most of what is currently known about T-cell receptor (TCR) signaling. However, many aspects of the genome modification of this cell line have not yet been analyzed. To identify genes of potential biological and clinical relevance in acute T-lymphoblastic leukemia (T-ALL), we performed an array comparative genomic hybridization (aCGH) approach on the widely used Jurkat cell line and examined the association of the detected copy number alterations (CNAs) with cancer hallmarks and T-ALL pathogenesis.<br />Materials and Methods: Cells were harvested by using trypsin/EDTA from culture flasks to extract genomic DNA. aCGH experiments were performed on an Agilent microarray platform using the SurePrint G3 Cancer CGH + SNP Microarray 4×180 K. Functional enrichment analysis of all CNAs was performed with the R package g:Profiler2. The association of these alterations with key cancer hallmarks was analyzed using the Cancer Hallmarks web-tool.<br />Results: Our analysis revealed several novel CNAs, including losses at 5p15.2, 6q27, 10q22.2, 14q11.2, 18q11.2-q12.1, and Xp22.33, as well as gains at 2p11.2, 7p21.2, 7q21.2 and 18p11.32. Genes within these regions were associated with important oncogenic pathways, including 'sustained proliferative signaling', 'tumor suppressor evasion', and 'angiogenesis promotion'.<br />Conclusion: These findings suggest that Jurkat cells may serve as a valuable model for identifying new targets for cancer research. Further studies are required to confirm the phenotypic implications of these variants, which may open new avenues for exploring the functional impact of these alterations and their potential role in the development of therapies.<br /> (Copyright © 2025, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)
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  Label: References
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  Data: Nucleic Acids Res. 2018 Jan 4;46(D1):D1144-D1149. (PMID: <searchLink fieldCode="PM" term="%2229099951%22">29099951)</searchLink><br />J Clin Invest. 2012 Oct;122(10):3398-406. (PMID: <searchLink fieldCode="PM" term="%2223023710%22">23023710)</searchLink><br />Cancers (Basel). 2020 Jul 20;12(7):. (PMID: <searchLink fieldCode="PM" term="%2232698360%22">32698360)</searchLink><br />Nat Rev Immunol. 2004 Apr;4(4):301-8. (PMID: <searchLink fieldCode="PM" term="%2215057788%22">15057788)</searchLink><br />Exp Mol Med. 2019 Jan 11;51(1):1-15. (PMID: <searchLink fieldCode="PM" term="%2230635552%22">30635552)</searchLink><br />BioData Min. 2013 Oct 16;6(1):18. (PMID: <searchLink fieldCode="PM" term="%2224131735%22">24131735)</searchLink><br />Anticancer Res. 2019 Dec;39(12):6443-6455. (PMID: <searchLink fieldCode="PM" term="%2231810908%22">31810908)</searchLink><br />Nature. 2017 Jun 15;546(7658):426-430. (PMID: <searchLink fieldCode="PM" term="%2228607489%22">28607489)</searchLink><br />Exp Cell Res. 1987 Aug;171(2):389-403. (PMID: <searchLink fieldCode="PM" term="%223476309%22">3476309)</searchLink><br />Nucleic Acids Res. 2021 Jan 8;49(D1):D1289-D1301. (PMID: <searchLink fieldCode="PM" term="%2233179738%22">33179738)</searchLink><br />Am J Respir Crit Care Med. 2019 Oct 1;200(7):888-899. (PMID: <searchLink fieldCode="PM" term="%2231166114%22">31166114)</searchLink><br />ACS Omega. 2020 Oct 14;5(42):27480-27491. (PMID: <searchLink fieldCode="PM" term="%2233134711%22">33134711)</searchLink><br />J Hematol Oncol. 2016 Oct 24;9(1):114. (PMID: <searchLink fieldCode="PM" term="%2227776559%22">27776559)</searchLink><br />Lancet. 2020 Apr 4;395(10230):1146-1162. (PMID: <searchLink fieldCode="PM" term="%2232247396%22">32247396)</searchLink><br />Mol Cancer Res. 2016 Jan;14(1):3-13. (PMID: <searchLink fieldCode="PM" term="%2226248648%22">26248648)</searchLink><br />Nature. 2019 May;569(7757):503-508. (PMID: <searchLink fieldCode="PM" term="%2231068700%22">31068700)</searchLink><br />Cell Rep. 2018 Apr 3;23(1):227-238.e3. (PMID: <searchLink fieldCode="PM" term="%2229617662%22">29617662)</searchLink><br />F1000Res. 2020 Jul 15;9:. (PMID: <searchLink fieldCode="PM" term="%2233564394%22">33564394)</searchLink><br />Leukemia. 2023 Mar;37(3):529-538. (PMID: <searchLink fieldCode="PM" term="%2236550215%22">36550215)</searchLink><br />Cancers (Basel). 2019 Dec 05;11(12):. (PMID: <searchLink fieldCode="PM" term="%2231817502%22">31817502)</searchLink><br />Nat Rev Clin Oncol. 2013 Mar;10(3):143-53. (PMID: <searchLink fieldCode="PM" term="%2223400000%22">23400000)</searchLink><br />Cancers (Basel). 2020 Jan 03;12(1):. (PMID: <searchLink fieldCode="PM" term="%2231947841%22">31947841)</searchLink><br />Mol Biol Rep. 2020 Jun;47(6):4587-4629. (PMID: <searchLink fieldCode="PM" term="%2232333246%22">32333246)</searchLink><br />Cancers (Basel). 2018 Apr 07;10(4):. (PMID: <searchLink fieldCode="PM" term="%2229642462%22">29642462)</searchLink><br />Cancers (Basel). 2019 Aug 01;11(8):. (PMID: <searchLink fieldCode="PM" term="%2231374935%22">31374935)</searchLink><br />Int J Cancer. 2020 Dec 1;147(11):2988-2995. (PMID: <searchLink fieldCode="PM" term="%2232406095%22">32406095)</searchLink><br />Oncotarget. 2015 Apr 30;6(12):10175-94. (PMID: <searchLink fieldCode="PM" term="%2225868388%22">25868388)</searchLink><br />Anticancer Res. 2019 Sep;39(9):4743-4748. (PMID: <searchLink fieldCode="PM" term="%2231519574%22">31519574)</searchLink><br />J Pharm Anal. 2025 May;15(5):101065. (PMID: <searchLink fieldCode="PM" term="%2240496069%22">40496069)</searchLink><br />J Mater Chem B. 2017 Jun 7;5(21):3970-3981. (PMID: <searchLink fieldCode="PM" term="%2232264258%22">32264258)</searchLink><br />Int J Cancer. 1977 May 15;19(5):621-6. (PMID: <searchLink fieldCode="PM" term="%2268013%22">68013)</searchLink><br />BMC Genomics. 2018 May 8;19(1):334. (PMID: <searchLink fieldCode="PM" term="%2229739316%22">29739316)</searchLink><br />Genes (Basel). 2021 Jul 23;12(8):. (PMID: <searchLink fieldCode="PM" term="%2234440292%22">34440292)</searchLink><br />Cancer Res. 2019 Nov 15;79(22):5734-5745. (PMID: <searchLink fieldCode="PM" term="%2231391186%22">31391186)</searchLink>
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