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  1 / 427 MEDLINE  
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[PMID]:29374701
[Au] Autor:Greco M; Arcidiacono B; Chiefari E; Vitagliano T; Ciriaco AG; Brunetti FS; Cuda G; Brunetti A
[Ad] Endereço:Department of Clinical and Experimental Medicine, University "Magna Græcia" of Catanzaro, Catanzaro, Italy.
[Ti] Título:HMGA1 and MMP-11 Are Overexpressed in Human Non-melanoma Skin Cancer.
[So] Source:Anticancer Res;38(2):771-778, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The High-Mobility Group A1 (HMGA1) protein has been implicated in human malignancies, playing an important role in cancer proliferation, angiogenesis and metastasis. Increased HMGA1 expression has been found in skin mouse tumors, whereas Hmga1-null mice were protected against skin carcinogenesis. Here, we examined the expression of HMGA1 in human skin tumors, squamous cell carcinoma and basal cell carcinoma. MATERIALS AND METHODS: Tumor and normal skin tissues from 15 affected patients were surgically excised, and mRNA and protein extraction was performed. mRNA and protein content for both HMGA1 and MMP-11, a proteinase enzyme that plays a role in tumor development and progression, was measured by real-time PCR and western blotting, respectively. Data were analyzed by the SPSS software. RESULTS: HMGA1 mRNA and protein expression patterns were higher in neoplastic skin lesions, compared to normal skin (p<0.001). Similar results were observed for MMP-11. CONCLUSION: Our data confirm previous observations in mice studies, and suggest that HMGA1 and MMP-11 may play a key role in the proliferation and progression of skin tumors in humans.
[Mh] Termos MeSH primário: Proteína HMGA1a/biossíntese
Metaloproteinase 11 da Matriz/biossíntese
Neoplasias Cutâneas/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Feminino
Proteína HMGA1a/genética
Seres Humanos
Masculino
Metaloproteinase 11 da Matriz/genética
Meia-Idade
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
Neoplasias Cutâneas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 124544-67-8 (HMGA1a Protein); EC 3.4.24.- (MMP11 protein, human); EC 3.4.24.- (Matrix Metalloproteinase 11)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  2 / 427 MEDLINE  
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[PMID]:29262452
[Au] Autor:Zhang YL; Song XF; Duan YJ; Zhao RL
[Ad] Endereço:The third Department of Intensive Care Unit, the First Hospital of Shijiazhuang, Shijiazhuang 050011, China.
[Ti] Título:[Expression and correlation of -1 and 1 in laryngeal squamous cell carcinoma].
[So] Source:Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi;52(12):927-932, 2017 Dec 07.
[Is] ISSN:1673-0860
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the expressions of -1 1 . Immunohistochemistry and reverse transcription-polymer chain reaction (RT-PCR) were used to detect the expressions of 1 -1 47 - 21 ( ). . 13.0 . The positive expression rates of Fra-1 and HMGA1 proteins in laryngeal squamous cancer tissue were 48.9% and 53.2%, which were respectively higher than the rates of 19.0% for Fra-1 (χ(2)=5.416, <0.05) and of 23.8% for HMGA1 (χ(2)=5.083, <0.05) in adjacent tissues. The expression of -1 (t -1.079, -1.066 -1.067, P<0.05), (t -1.068 -1.054, P>0.05). 1 (t -1.112, -1.065, -1.009 -1.066, P<0.05), (t=-1.036, P>0.05). -1 1 (r=0.672, P<0.05). In laryngeal squamous cancer, -1 1 .
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/genética
Expressão Gênica
Proteína HMGA1a/genética
Neoplasias Laríngeas/genética
Proteínas Proto-Oncogênicas c-fos/genética
[Mh] Termos MeSH secundário: Adulto
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/patologia
Carcinoma de Células Escamosas/secundário
Proteína HMGA1a/metabolismo
Seres Humanos
Imuno-Histoquímica
Neoplasias Laríngeas/metabolismo
Neoplasias Laríngeas/patologia
Metástase Linfática
Proteínas Proto-Oncogênicas c-fos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-fos); 0 (fos-related antigen 1); 124544-67-8 (HMGA1a Protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1673-0860.2017.12.010


  3 / 427 MEDLINE  
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[PMID]:28481878
[Au] Autor:Maurus K; Hufnagel A; Geiger F; Graf S; Berking C; Heinemann A; Paschen A; Kneitz S; Stigloher C; Geissinger E; Otto C; Bosserhoff A; Schartl M; Meierjohann S
[Ad] Endereço:Department of Physiological Chemistry, University of Würzburg, Würzburg, Germany.
[Ti] Título:The AP-1 transcription factor FOSL1 causes melanocyte reprogramming and transformation.
[So] Source:Oncogene;36(36):5110-5121, 2017 Sep 07.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The MAPK pathway is activated in the majority of melanomas and is the target of therapeutic approaches. Under normal conditions, it initiates the so-called immediate early response, which encompasses the transient transcription of several genes belonging to the AP-1 transcription factor family. Under pathological conditions, such as continuous MAPK pathway overactivation due to oncogenic alterations occurring in melanoma, these genes are constitutively expressed. The consequences of a permanent expression of these genes are largely unknown. Here, we show that FOSL1 is the main immediate early AP-1 member induced by melanoma oncogenes. We first examined its role in established melanoma cells. We found that FOSL1 is involved in melanoma cell migration as well as cell proliferation and anoikis-independent growth, which is mediated by the gene product of its target gene HMGA1, encoding a multipotent chromatin modifier. As FOSL1 expression is increased in patient melanoma samples compared to nevi, we investigated the effect of enhanced FOSL1 expression on melanocytes. Intriguingly, we found that FOSL1 acts oncogenic and transforms melanocytes, enabling subcutaneous tumor growth in vivo. During the process of transformation, FOSL1 reprogrammed the melanocytes and downregulated MITF in a HMGA1-dependent manner. At the same time, AXL was upregulated, leading to a shift in the MITF/AXL balance. Furthermore, FOSL1 re-enforced pro-tumorigenic transcription factors MYC, E2F3 and AP-1. Together, this led to the enhancement of several growth-promoting processes, such as ribosome biogenesis, cellular detachment and pyrimidine metabolism. Overall, we demonstrate that FOSL1 is a novel reprogramming factor for melanocytes with potent tumor transformation potential.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/patologia
Regulação Neoplásica da Expressão Gênica
Melanócitos/patologia
Melanoma/patologia
Proteínas Proto-Oncogênicas c-fos/metabolismo
Neoplasias Cutâneas/patologia
Fator de Transcrição AP-1/metabolismo
[Mh] Termos MeSH secundário: Movimento Celular
Proliferação Celular
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Células Cultivadas
Perfilação da Expressão Gênica
Proteína HMGA1a/genética
Proteína HMGA1a/metabolismo
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Melanócitos/metabolismo
Melanoma/genética
Melanoma/metabolismo
Fator de Transcrição Associado à Microftalmia/genética
Fator de Transcrição Associado à Microftalmia/metabolismo
Nevo/genética
Nevo/metabolismo
Nevo/patologia
Proteínas Proto-Oncogênicas c-fos/genética
Transdução de Sinais
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/metabolismo
Fator de Transcrição AP-1/genética
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MITF protein, human); 0 (Microphthalmia-Associated Transcription Factor); 0 (Proto-Oncogene Proteins c-fos); 0 (Transcription Factor AP-1); 0 (fos-related antigen 1); 124544-67-8 (HMGA1a Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.135


  4 / 427 MEDLINE  
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[PMID]:28393241
[Au] Autor:Zhong J; Liu C; Zhang QH; Chen L; Shen YY; Chen YJ; Zeng X; Zu XY; Cao RX
[Ad] Endereço:Institute of Clinical Medicine, The First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, P.R. China.
[Ti] Título:TGF-ß1 induces HMGA1 expression: The role of HMGA1 in thyroid cancer proliferation and invasion.
[So] Source:Int J Oncol;50(5):1567-1578, 2017 May.
[Is] ISSN:1791-2423
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:The role of transforming growth factor-ß1 (TGF-ß1) is complicated and plays a different role in the development of cancer. High mobility group A (HMGA1) participates in multiple cellular biology processes, and exerts important roles in the epithelial-mesenchymal transition (EMT). However, the correlation of TGF-ß1 and HMGA1 in cancer cells is not yet fully understood. In this study, we determined the effects of TGF-ß1 on HMGA1 expression in thyroid cancer cells and examined the role of HMGA1 in thyroid cancer progression. With real-time PCR and immunofluorescence staining, our study demonstrated that TGF-ß1 induced the expression of HMGA1 through phosphoinositide 3-kinase (PI3K) and the extracellular signal-related kinase (ERK) signaling in thyroid cancer cells. With luciferase reported assay, the HMGA1 promoter activity was activated by TGF-ß1 in the SW579 cells. Furthermore, lentivirus-mediated HMGA1 knockdown inhibits cellular oncogenic properties of thyroid cancer cells. Clinically, tissue microarray revealed that HMGA1 was expressed in thyroid carcinoma more than that in normal thyroid tissues (P<0.001); expression of HMGA1 and MMP-2 was identified to be positively correlated (P=0.017). The present study established the first link between HMGA1 and TGF-ß1 in the regulation of thyroid cancer proliferation and invasion, and provided evidence for the pivotal role of HMGA1 in the progression of thyroid cancer, indicating HMGA1 to be potential biological marker for the diagnosis of thyroid cancer.
[Mh] Termos MeSH primário: Proteína HMGA1a/genética
Metaloproteinase 2 da Matriz/genética
Neoplasias da Glândula Tireoide/genética
Fator de Crescimento Transformador beta1/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Proteína HMGA1a/biossíntese
Seres Humanos
Sistema de Sinalização das MAP Quinases
Masculino
Metaloproteinase 2 da Matriz/biossíntese
Meia-Idade
Invasividade Neoplásica/genética
Neoplasias da Glândula Tireoide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transforming Growth Factor beta1); 124544-67-8 (HMGA1a Protein); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.3892/ijo.2017.3958


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[PMID]:28358427
[Au] Autor:Yang Q; Wang X; Tang C; Chen X; He J
[Ad] Endereço:Department of General Surgery, The Affiliated Hospital, Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
[Ti] Título:H19 promotes the migration and invasion of colon cancer by sponging miR-138 to upregulate the expression of HMGA1.
[So] Source:Int J Oncol;50(5):1801-1809, 2017 May.
[Is] ISSN:1791-2423
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Colon cancer is the most common digestive system malignancy, along with high mortality rate, familial transmissibility and hepatic metastasis. Our study investigated the role of long non-coding RNA H19 in colon cancer. We found that H19 was overexpressed in colon cancer tissues and cell lines, the interference of H19 by short hairpin RNA (shRNA) effectively decreased the migration and invasion of colon cancer cells (HT-29 and RKO). Besides, miR-138 was predicted a target of H19, and low expression of miR-138 was found in colon cancer tissues and cells. The silence of H19 strongly increased the expression of miR-138. The decreased level of miR-138 was elevated adding miR-138 mimic in RKO cells transfected with lncRNA-H19. Similarly, the upregulated level of miR-138 was downregulated adding miR-138 inhibitor in RKO cells transfected with H19 shRNA. The luciferase reporter confirmed the targeting reaction between H19 and miR-138. Moreover, the high-mobility group A (HMGA1) protein was predicted as a target of miR-138. HMGA1 was suppressed by H19 shRNA and could be up-regulated by miR-138 inhibitor. The migration and invasion ability of colon cancer was restrained by H19 shRNA and promoted by miR-138 inhibitor. Finally, the in vivo experiment revealed that H19 shRNA strongly reduced the tumor growth and tumor volume. H19 shRNA also inhibited metastasis via suppressing hepatic metastases and the expression of metastasis-related proteins. Taken together, our research indicated an H19-miR138-HMGA1 pathway in regulating the migration and invasion of colon cancer, providing new insight for treatment of colon cancer.
[Mh] Termos MeSH primário: Neoplasias do Colo/genética
Proteína HMGA1a/biossíntese
MicroRNAs/genética
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Neoplasias do Colo/patologia
Feminino
Regulação Neoplásica da Expressão Gênica
Proteína HMGA1a/genética
Seres Humanos
Masculino
Camundongos
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
RNA Interferente Pequeno
Ativação Transcricional
Transfecção
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (H19 long non-coding RNA); 0 (MIRN138 microRNA, human); 0 (MicroRNAs); 0 (RNA, Long Noncoding); 0 (RNA, Small Interfering); 124544-67-8 (HMGA1a Protein)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170720
[Lr] Data última revisão:
170720
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.3892/ijo.2017.3941


  6 / 427 MEDLINE  
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[PMID]:28255268
[Au] Autor:Qiu H; Zhong J; Luo L; Tang Z; Liu N; Kang K; Li L; Gou D
[Ad] Endereço:Shenzhen Key Laboratory of Microbial Genetic Engineering, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong, 518060, China.; Key Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province, College of Optoelectronic Engineering, Shenzhen Universi
[Ti] Título:Regulatory Axis of miR-195/497 and HMGA1-Id3 Governs Muscle Cell Proliferation and Differentiation.
[So] Source:Int J Biol Sci;13(2):157-166, 2017.
[Is] ISSN:1449-2288
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Myocytes withdraw from the cell cycle to differentiate during muscle development. Given the capacity of microRNAs (miRNAs) to regulate gene expression during development, we screened for miRNAs that were associated with muscle development. S-Poly(T) Plus analysis of 273 miRNAs in porcine longissimus dorsi muscles revealed 14 miRNAs that were strongly upregulated with age of postnatal muscle development , including miR-195 and miR-497. These two miRNAs were also strongly upregulated at late differentiation stages of mouse skeletal myoblast C2C12 cells, and demethylation treatment induced significant upregulation of miR-195/497. Manipulation of miR-195/497 expression resulted in dramatic changes in the proliferation and differentiation of C2C12 cells. We identified high-mobility group AT-hook 1 ( ) mRNA as a highly conserved target of miR-195/497 in C2C12 myoblasts. Overexpression of miR-195/497 or silencing in C2C12 cells promoted myogenic differentiation. Moreover, we showed that miR-195/497 repressed , which in turn downregulated one of the HMGA1 downstream targets , whose inhibitory effect on myogenic differentiation is well established. Our study revealed a subset of potential development-associated miRNAs and suggests a novel regulatory axis for myogenesis in which miR-195/497 promote myogenic differentiation by repressing the HMGA1-Id3 pathway.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Proliferação Celular/fisiologia
Proteínas HMGA/metabolismo
MicroRNAs/genética
Desenvolvimento Muscular/fisiologia
Mioblastos/citologia
Mioblastos/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Regiões 3' não Traduzidas/fisiologia
Animais
Western Blotting
Diferenciação Celular/genética
Linhagem Celular
Proliferação Celular/genética
Proteínas HMGA/genética
Proteína HMGA1a/genética
Proteína HMGA1a/metabolismo
Seres Humanos
Masculino
Camundongos
MicroRNAs/metabolismo
MicroRNAs/fisiologia
Desenvolvimento Muscular/genética
Plasmídeos/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (HMGA Proteins); 0 (MIRN195 microRNA, human); 0 (MIRN497 microRNA, human); 0 (MicroRNAs); 124544-67-8 (HMGA1a Protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE
[do] DOI:10.7150/ijbs.17440


  7 / 427 MEDLINE  
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[PMID]:28000891
[Au] Autor:Sekimoto N; Suzuki A; Suzuki Y; Sugano S
[Ad] Endereço:Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo 108­8639, Japan.
[Ti] Título:Expression of miR­26a exhibits a negative correlation with HMGA1 and regulates cancer progression by targeting HMGA1 in lung adenocarcinoma cells.
[So] Source:Mol Med Rep;15(2):534-542, 2017 Feb.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Lung cancer is the most common cause of cancer­associated mortality worldwide, and the number of cases is increasing annually. Several studies have shown that microRNAs (miRNAs) control proliferation, differentiation, and apoptosis in various cell types, and increasing evidence indicates the presence of aberrant miRNA expression profiles and unique miRNA signaling pathways in several types of cancer. The present study aimed to identify miRNAs, which correlated specifically with the progression of lung cancer through the analysis of 57,100 transcripts and 1,341 small RNA expression profiles in 26 lung adenocarcinoma cell lines using next­generation sequencing. The most marked negative correlation was found between the expression of hsa­miR­26a­1 and messenger RNA (mRNA), and a list of mRNAs, which exhibited negative correlation with hsa­miR­26a­1 were investigated. The most marked negative correlation was observed between the expression levels of hsa­miR­26a­1 and high mobility group A1 (HMGA1). Using a lung adenocarcinoma cell line, the present study analyzed the effect of the overexpression of miR­26a on the expression of HMGA1 and found that miR­26a repressed the expression of HMGA1 by reducing the mRNA levels of HMGA1. Furthermore, it was demonstrated that the overexpression of miR­26a in a lung adenocarcinoma cell line repressed cell migration, invasion and growth by targeting HMGA1. Taken together, the present study showed a significant negative correlation between the expression of miR­26a and HMGA1 in 26 lung adenocarcinoma cell lines, and provided evidence that the suppression of miR­26a supports the progression of cancer by stimulating the expression of HMGA1.
[Mh] Termos MeSH primário: Proteína HMGA1a/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Sequência de Bases
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Proteína HMGA1a/antagonistas & inibidores
Proteína HMGA1a/genética
Seres Humanos
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/patologia
MicroRNAs/genética
PTEN Fosfo-Hidrolase/metabolismo
Interferência de RNA
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/metabolismo
Alinhamento de Sequência
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 124544-67-8 (HMGA1a Protein); EC 3.1.3.67 (PTEN Phosphohydrolase)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161222
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2016.6053


  8 / 427 MEDLINE  
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[PMID]:27839822
[Au] Autor:De Rosa S; Chiefari E; Salerno N; Ventura V; D'Ascoli GL; Arcidiacono B; Ambrosio G; Bilotta FL; Torella D; Foti D; Indolfi C; Brunetti A
[Ad] Endereço:Division of Cardiology, Department of Medical and Surgical Sciences, "Magna Graecia" University, Catanzaro, Italy.
[Ti] Título:HMGA1 is a novel candidate gene for myocardial infarction susceptibility.
[So] Source:Int J Cardiol;227:331-334, 2017 Jan 15.
[Is] ISSN:1874-1754
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute Myocardial infarction (AMI), a leading cause of morbidity and mortality worldwide, is a dreadful acute complication of coronary atherosclerosis. Type 2 diabetes mellitus (T2DM) is associated with an increased risk of developing AMI. The architectural transcription factor high-mobility-group AT-hook 1 (HMGA1) has been involved in atherosclerosis, plaque formation, inflammation, and in the pathogenesis of insulin resistance and T2DM. An association of the HMGA1 rs146052672 variant with T2DM has been recently reported. Thus, our aim was to evaluate whether this variant was also associated with AMI. METHODS AND RESULTS: In a case-control study from Calabria (Southern Italy), we enrolled 254 consecutive, unrelated, patients with first diagnosis of AMI, and 508 age, sex-matched controls. Genotyping of the rs146052672 was performed using the TaqMan allelic discrimination method. We found that this variant was present in 7.9% of AMI patients and in 3.1% of controls (p=0.003). Multiple logistic regression confirmed that the rs146052672 was significantly associated with AMI (OR=2.54; p=0.002), and this association was independent of classical cardiovascular risk factors such as gender, hypertension, obesity and T2DM (for all, p<0.05). CONCLUSIONS: Our findings demonstrate that a relationship exists between the HMGA1 rs146052672 variant and AMI, suggesting that defects at the HMGA1 locus may play a pathogenetic role in AMI, in the absence of T2DM and other cardiovascular risk factors.
[Mh] Termos MeSH primário: Predisposição Genética para Doença/genética
Proteína HMGA1a/genética
Infarto do Miocárdio/genética
[Mh] Termos MeSH secundário: Idoso
Estudos de Casos e Controles
Feminino
Genótipo
Seres Humanos
Itália
Masculino
Meia-Idade
Polimorfismo Genético/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
124544-67-8 (HMGA1a Protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161115
[St] Status:MEDLINE


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[PMID]:26923360
[Au] Autor:Akhter MZ; Rajeswari MR
[Ad] Endereço:a Department of Biochemistry , All India Institute of Medical Sciences , New Delhi - 110029 , India.
[Ti] Título:Triplex forming oligonucleotides targeted to hmga1 selectively inhibit its expression and induce apoptosis in human cervical cancer.
[So] Source:J Biomol Struct Dyn;35(4):689-703, 2017 Mar.
[Is] ISSN:1538-0254
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:High-mobility group A1 (HMGA1) is a non-histone chromosomal protein, which is known as 'architectural' transcription factor that facilitates the assembly of 'enhanceosome.' Because of its elevated expression in a number of human malignancies, with barely minimal levels in healthy adults, HMGA1 is considered as potential 'tumor marker.' Therefore, we looked at the inhibition of hmga1 using anti-gene strategy, as an attractive therapeutic approach. This was achieved by two triplex forming oligonucleotides (TFOs), TFO1 and TFO2 targeted to the promoter of hmga1 at positions, -284--304 and -2800--2826, respectively. The stability of two DNA triplexes was characterized using a variety of biophysical and thermodynamics techniques and was confirmed by gel retardation assay using γ- P [ATP]. The efficacy of TFOs on HMGA1 expression was evaluated in HeLa cells using MTT assay, Flow cytometry, Western blot, and RT-PCR. Results revealed that DNA Triplex1 formed by TFO1 is more stable and stronger than the corresponding Triplex2. Although both TFOs downregulated hmga1 expression at mRNA and protein levels and caused apoptotic cell death in HeLa cell line, TFO1 demonstrated a greater effect at low concentration which corroborates well with the stability data. Thus, TFO-mediated inhibition of hmga1 expression can be a promising strategy for the development of novel anti-cancer therapeutics.
[Mh] Termos MeSH primário: Apoptose/genética
DNA/genética
Proteína HMGA1a/antagonistas & inibidores
Oligonucleotídeos/genética
Regiões Promotoras Genéticas/genética
Neoplasias do Colo do Útero/genética
Neoplasias do Colo do Útero/patologia
[Mh] Termos MeSH secundário: Adulto
Sequência de Bases
Feminino
Proteína HMGA1a/genética
Seres Humanos
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oligonucleotides); 0 (triplex DNA); 124544-67-8 (HMGA1a Protein); 9007-49-2 (DNA)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170404
[Lr] Data última revisão:
170404
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160301
[St] Status:MEDLINE
[do] DOI:10.1080/07391102.2016.1160257


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[PMID]:27723831
[Au] Autor:Pellarin I; Arnoldo L; Costantini S; Pegoraro S; Ros G; Penzo C; Triolo G; Demarchi F; Sgarra R; Vindigni A; Manfioletti G
[Ad] Endereço:Department of Life Sciences, University of Trieste, Trieste, Italy.
[Ti] Título:The Architectural Chromatin Factor High Mobility Group A1 Enhances DNA Ligase IV Activity Influencing DNA Repair.
[So] Source:PLoS One;11(10):e0164258, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The HMGA1 architectural transcription factor is an oncogene overexpressed in the vast majority of human cancers. HMGA1 is a highly connected node in the nuclear molecular network and the key aspect of HMGA1 involvement in cancer development is that HMGA1 simultaneously confers cells multiple oncogenic hits, ranging from global chromatin structural and gene expression modifications up to the direct functional alterations of key cellular proteins. Interestingly, HMGA1 also modulates DNA damage repair pathways. In this work, we provide evidences linking HMGA1 with Non-Homologous End Joining DNA repair. We show that HMGA1 is in complex with and is a substrate for DNA-PK. HMGA1 enhances Ligase IV activity and it counteracts the repressive histone H1 activity towards DNA ends ligation. Moreover, breast cancer cells overexpressing HMGA1 show a faster recovery upon induction of DNA double-strand breaks, which is associated with a higher survival. These data suggest that resistance to DNA-damaging agents in cancer cells could be partially attributed to HMGA1 overexpression thus highlighting the relevance of considering HMGA1 expression levels in the selection of valuable and effective pharmacological regimens.
[Mh] Termos MeSH primário: Cromatina/química
DNA Ligase Dependente de ATP/metabolismo
Reparo do DNA
Proteína HMGA1a/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Cromatina/metabolismo
Cromatografia Líquida de Alta Pressão
Ensaio Cometa
Proteína HMGA1a/genética
Proteína HMGA2/genética
Proteína HMGA2/metabolismo
Histonas/metabolismo
Seres Humanos
Autoantígeno Ku/metabolismo
Células MCF-7
Microscopia de Fluorescência
Fosforilação
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/química
Proteínas Recombinantes/isolamento & purificação
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (HMGA2 Protein); 0 (Histones); 0 (Recombinant Proteins); 124544-67-8 (HMGA1a Protein); EC 4.2.99.- (Ku Autoantigen); EC 6.5.1.1 (DNA Ligase ATP)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0164258



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