HMGA proteins promote ATM expression and enhance cancer cell resistance to genotoxic agents (1130 views)
Oncogene (ISSN: 0950-9232, 1476-5594), 2011 Jul 7; 30(27): 3024-3035.
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Paper type: Journal Article,
Impact factor: 6.373, 5-year impact factor: 6.889
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-79960065049&partnerID=40&md5=12e3e2f10e8021ad1d67de4df0692e7d
Keywords: Atm, Dna Repair, Hmga, Actin, Atm Protein, High Mobility Group A Protein, High Mobility Group A1 Protein, High Mobility Group A2 Protein, Protein P21, Unclassified Drug, Vinculin, Animal Cell, Article, Atm Gene, Cancer Relapse, Cancer Resistance, Cell Stress, Cell Transformation, Controlled Study, Dna Damage, Embryo, Enzyme Induction, Gene Expression, Genotoxicity, Human, Human Cell, Mouse, Nonhuman, Positive Feedback, Priority Journal, Prognosis, Promoter Region, Protein Expression, Protein Family, Transcription Initiation, Cell Cycle Proteins, Cell Line, Dna-Binding Proteins, Gene Expression Regulation, Neoplastic, Hmga Proteins, Mutagens, Phosphorylation, Genetic, Protein-Serine-Threonine Kinases, Tumor Suppressor Proteins, Ataxia Telangiectasia,
Affiliations:
*** IBB - CNR ***
Dipartimento di Biologia e Patologia Cellulare e Molecolare, Istituto di Endocrinologia Ed Oncologia Sperimentale Del CNR, Università Degli Studi di Napoli Federico II, Via Pansini 5, 80131 Napoli, Italy
Istituto di Biostrutture e Bioimmagini Del CNR, Naples, Italy
Department of Molecular Virology, Immunology and Medical Genetics, Comprehensive Cancer Center, Ohio State University, Columbus, OH, United States
NOGEC (Naples Oncogenomic Center), CEINGE Biotecnologie Avanzate, Via Comunale Margherita, Naples, Italy
References:
Not available.
Oncogene (ISSN: 0950-9232, 1476-5594), 2011 Jul 7; 30(27): 3024-3035.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 6.373, 5-year impact factor: 6.889
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-79960065049&partnerID=40&md5=12e3e2f10e8021ad1d67de4df0692e7d
Keywords: Atm, Dna Repair, Hmga, Actin, Atm Protein, High Mobility Group A Protein, High Mobility Group A1 Protein, High Mobility Group A2 Protein, Protein P21, Unclassified Drug, Vinculin, Animal Cell, Article, Atm Gene, Cancer Relapse, Cancer Resistance, Cell Stress, Cell Transformation, Controlled Study, Dna Damage, Embryo, Enzyme Induction, Gene Expression, Genotoxicity, Human, Human Cell, Mouse, Nonhuman, Positive Feedback, Priority Journal, Prognosis, Promoter Region, Protein Expression, Protein Family, Transcription Initiation, Cell Cycle Proteins, Cell Line, Dna-Binding Proteins, Gene Expression Regulation, Neoplastic, Hmga Proteins, Mutagens, Phosphorylation, Genetic, Protein-Serine-Threonine Kinases, Tumor Suppressor Proteins, Ataxia Telangiectasia,
Affiliations:
*** IBB - CNR ***
Dipartimento di Biologia e Patologia Cellulare e Molecolare, Istituto di Endocrinologia Ed Oncologia Sperimentale Del CNR, Università Degli Studi di Napoli Federico II, Via Pansini 5, 80131 Napoli, Italy
Istituto di Biostrutture e Bioimmagini Del CNR, Naples, Italy
Department of Molecular Virology, Immunology and Medical Genetics, Comprehensive Cancer Center, Ohio State University, Columbus, OH, United States
NOGEC (Naples Oncogenomic Center), CEINGE Biotecnologie Avanzate, Via Comunale Margherita, Naples, Italy
References:
Not available.
HMGA proteins promote ATM expression and enhance cancer cell resistance to genotoxic agents
DNA-damaging therapies represent a keystone in cancer treatment. Unfortunately, many tumors often relapse because of a group of cancer cells, which are resistant to conventional therapies. High-mobility group A (HMGA) proteins has a key role in cell transformation, and their overexpression is a common feature of human malignant neoplasias, representing a poor prognostic index often correlated to anti-cancer drug resistance. Our previous results demonstrated that HMGA1 is a substrate of ataxia-telangiectasia mutated (ATM), the main cellular sensor of genotoxic stress. Here we also report thatHMGA2, the other member of the HMGA family, is a novel substrate of ATM. Interestingly, we found that HMGA proteins positively regulate ATM gene expression. Moreover, induction of ATM kinase activity by DNA-damaging agents enhances HMGA-dependent transcriptional activation of ATM promoter, suggesting that ATM expression is modulated by a DNA-damage- and HMGA-dependent positive feedback loop. Finally, inhibition of HMGA expression in mouse embryonic fibroblasts and in cancer cells strongly reduces ATM protein levels, impairing the cellular DNA-damage response and enhancing the sensitivity to DNA-damaging agents. These findings indicate this novel HMGA-ATM pathway as a new potential target to improve the effectiveness of conventional anti-neoplastic treatments on the genotoxic-drug resistant cancer cells. © 2011 Macmillan Publishers Limited All rights reserved.
DNA-damaging therapies represent a keystone in cancer treatment. Unfortunately, many tumors often relapse because of a group of cancer cells, which are resistant to conventional therapies. High-mobility group A (HMGA) proteins has a key role in cell transformation, and their overexpression is a common feature of human malignant neoplasias, representing a poor prognostic index often correlated to anti-cancer drug resistance. Our previous results demonstrated that HMGA1 is a substrate of ataxia-telangiectasia mutated (ATM), the main cellular sensor of genotoxic stress. Here we also report thatHMGA2, the other member of the HMGA family, is a novel substrate of ATM. Interestingly, we found that HMGA proteins positively regulate ATM gene expression. Moreover, induction of ATM kinase activity by DNA-damaging agents enhances HMGA-dependent transcriptional activation of ATM promoter, suggesting that ATM expression is modulated by a DNA-damage- and HMGA-dependent positive feedback loop. Finally, inhibition of HMGA expression in mouse embryonic fibroblasts and in cancer cells strongly reduces ATM protein levels, impairing the cellular DNA-damage response and enhancing the sensitivity to DNA-damaging agents. These findings indicate this novel HMGA-ATM pathway as a new potential target to improve the effectiveness of conventional anti-neoplastic treatments on the genotoxic-drug resistant cancer cells. © 2011 Macmillan Publishers Limited All rights reserved.
HMGA proteins promote ATM expression and enhance cancer cell resistance to genotoxic agents
| ▼ Biochemical and structural insights on Chromatin Assembly Factor 1 in physio/pathological events |
HMGA proteins promote ATM expression and enhance cancer cell resistance to genotoxic agents
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View Export to BibTeX Export to EndNote
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View Export to BibTeX Export to EndNote
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View Export to BibTeX Export to EndNote
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Merolla F, Pentimalli F, Pacelli R, Vecchio G, Fusco A, Grieco M, Celetti A
* Involvement of H4(D10S170) protein in ATM-dependent response to DNA damage (749 views)
Oncogene (ISSN: 0950-9232, 1476-5594), 2007 Sep 13; 26(42): 6167-6175.
Impact Factor: 6.44
View Export to BibTeX Export to EndNote
Copani A, Caraci F, Hoozemans J, Calafiore M, Sortino M, Nicoletti F
* The nature of the cell cycle in neurons: Focus on a "non-canonical" pathway of DNA replication causally related to death (707 views)
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View Export to BibTeX Export to EndNote
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Impact Factor: 2.117
View Export to BibTeX Export to EndNote
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View Export to BibTeX Export to EndNote
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View Export to BibTeX Export to EndNote
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View Export to BibTeX Export to EndNote
21 Records (20 excluding Abstracts).
Total impact factor: 104.462 (100.732 excluding Abstracts).
Total 5 year impact factor: 102.306 (98.062 excluding Abstracts).
Total impact factor: 104.462 (100.732 excluding Abstracts).
Total 5 year impact factor: 102.306 (98.062 excluding Abstracts).
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