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  1 / 20 LILACS  
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Id: biblio-838968
Autor: Gan, Zhihua; Han, Kun; Lin, Shuchen; Hu, Haiyan; Shen, Zan; Min, Daliu.
Título: Knockdown of ubiquitin-specific peptidase 39 inhibited the growth of osteosarcoma cells and induced apoptosis in vitro
Fonte: Biol. Res;50:15, 2017. graf.
Idioma: en.
Projeto: National Nature Science Foundation of China; . National Nature Science Foundation of China.
Resumo: BACKGROUND: Ubiquitin specific peptidase 39 (USP39), an essential factor in the assembly of the mature spliceosome complex, has an aberrant expression in several cancer. However, its function and the corresponding mechanism on human osteosarcoma has not been fully explored yet. METHODS: The mRNA and DNA copies of USP39 were increased in osteosarcoma cancer tissues compared with the one in human normal tissues according to datasets from the publicly available Oncomine database. A further western blot analysis also demonstrated an aberrant endogenous expression of USP39 in three different osteosarcoma cells. Then lentivirus-mediated short hairpin RNA (shRNA) was designed to silence USP39 in human osteosarcoma cell line U2OS, which is used to test the impact of USP39-silencing on cellular proliferation, colony formation, cell cycle distribution and apoptosis. RESULTS: Knockdown of USP39 expression in U2OS cell significantly decreased cell proliferation, impaired colony formation ability. A further analysis indicated suppression of USP39 arrested cell cycle progression at G2/M phase via p21 dependent way. In addition, the results of Annexin V/7-AAD staining suggested the knockdown of USP39 could promote U2OS cell apoptosis through PARP cleavage. CONCLUSIONS: These results uncover the critical role of USP39 in regulating cancer cell mitosis and indicate USP39 is critical for osteosarcoma tumorigenesis.
Descritores: Osteossarcoma/enzimologia
Osteossarcoma/patologia
Apoptose
Técnicas de Silenciamento de Genes/métodos
Proteases Específicas de Ubiquitina/metabolismo
-Ensaio Tumoral de Célula-Tronco
Regulação Neoplásica da Expressão Gênica
Lentivirus
Linhagem Celular Tumoral
Proliferação de Células
Proteases Específicas de Ubiquitina/genética
Citometria de Fluxo
Vetores Genéticos
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


  2 / 20 LILACS  
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Id: biblio-950787
Autor: Song, Bin; Bian, Qi; Shao, Cheng-Hao; Liu, An-An; Jing, Wei; Liu, Rui; Zhang, Yi-Jie; Zhou, Ying-Qi; Li, Gang; Jin, Gang.
Título: Sox2 function as a negative regulator to control HAMP expression
Fonte: Biol. Res;48:1-8, 2015. graf.
Idioma: en.
Projeto: Shanghai Municipal Natural Science Foundation.
Resumo: BACKGROUND: Hepcidin, encoding by HAMP gene, is the pivotal regulator of iron metabolism, controlling the systemic absorption and transportation of irons from intracellular stores. Abnormal levels of HAMP expression alter plasma iron parameters and lead to iron metabolism disorders. Therefore,itis animportant goal to understand the mechanisms controlling HAMP gene expression. RESULTS: Overexpression of Sox2 decrease basal expression of HAMP or induced by IL-6 or BMP-2, whereas, knockdown of Sox2 can increase HAMP expression, furthermore, two potential Sox2-binding sites were identified within the human HAMP promoter. Indeed, luciferase experiments demonstrated that deletion of any Sox2-binding site impaired the negative regulation of Sox2 on HAMP promoter transcriptional activity in basal conditions. ChIP experiments showed that Sox2 could directly bind to these sites. Finally, we verified the role of Sox2 to negatively regulate HAMP expression in human primary hepatocytes. CONCLUSION: We found that Sox2 as a novel factor to bind with HAMP promoter to negatively regulate HAMP expression, which may be further implicated as a therapeutic option for the amelioration of HAMP-overexpression-related diseases, including iron deficiency anemia.
Descritores: Regulação Neoplásica da Expressão Gênica/genética
Hepatócitos/metabolismo
Fatores de Transcrição SOXB1/genética
Hepcidinas/genética
-Plasmídeos/genética
Sítios de Ligação
Interleucina-6/metabolismo
Regiões Promotoras Genéticas/genética
Proteína Morfogenética Óssea 2/metabolismo
Fatores de Transcrição SOXB1/metabolismo
Técnicas de Silenciamento de Genes
Células Hep G2
Hepcidinas/metabolismo
Vetores Genéticos
Anemia/genética
Anemia/metabolismo
Ferro/metabolismo
Luciferases
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


  3 / 20 LILACS  
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Id: biblio-950819
Autor: Koriauli, S; Natsvlishvili, N; Barbakadze, T; Mikeladze, D.
Título: Knockdown of interleukin-10 induces the redistribution of sigma1-receptor and increases the glutamate-dependent NADPH-oxidase activity in mouse brain neurons
Fonte: Biol. Res;48:1-5, 2015. graf.
Idioma: en.
Resumo: BACKGROUND: In the central nervous system, interleukin-10 (IL-10) provides trophic and survival effects directly on neurons, modulates neurite plasticity, and has a pivotal importance in the neuronal regeneration in neurodegenerative and neuroinflammatory conditions. This cytokine is primarily produced by glial cells and has beneficial effects on the neuronal viability. However, the mechanisms of IL-10-elicited neuroprotection are not clear. RESULTS: Membrane preparations, isolated from wild-type (Wt) and IL-10 knockout (KO) mice brain were used in this study. It has been shown that compared to wild-type mice, in IL-10 KO mice brain, the amount of immunoglobulin binding protein (BiP) is greatly increased, whereas the content of sigma receptor-1 (SigR1) is not changed significantly. Co-immunoprecipitation experiments have shown that the association of SigR1 with small GTPase Rac1 (Ras-related C3 botulinum toxin substrate 1), NR2B subunit of NMDA-receptor (NMDAR) and inositol-3-phosphate receptor (IP3R) is higher in the IL-10 KO mice brain than in the Wt mice brain. Besides, we have found that either glutamate or sigma ligands, separately or together, do not change glutamate-induced NADPH-oxidase (NOX) activity in Wt-type mice brain membrane preparations, whereas in IL-10 KO mice high concentration of glutamate markedly increases the NOX-dependent production of reactive oxygen species (ROS). Glutamate-dependent ROS production was decreased to the normal levels by the action of sigma-agonists. CONCLUSIONS: It has been concluded that IL-10 deprivation, at least in part, can lead to the induction of ER-stress, which causes BiP expression and SigR1 redistribution between components of endoplasmic reticulum (ER) and plasma membrane. Moreover, IL-10 deficiency can change the specific organization of NMDAR, increasing the surface expression of SigR1-sensitive NR2B-containing NMDAR. In these conditions, glutamate-dependent ROS production is greatly increased leading to the initiation of apoptosis. In this circumstances, sigma-ligands could play a preventive role against NMDA receptor-mediated excitotoxicity.
Descritores: Encéfalo/metabolismo
Interleucina-10/genética
Receptores sigma/metabolismo
Ácido Glutâmico/metabolismo
NADPH Oxidases/metabolismo
-Membrana Celular/metabolismo
Receptores sigma/classificação
Receptores sigma/agonistas
Espécies Reativas de Oxigênio/análise
Espécies Reativas de Oxigênio/metabolismo
Receptores de N-Metil-D-Aspartato/classificação
Receptores de N-Metil-D-Aspartato/metabolismo
Proteínas rac1 de Ligação ao GTP/metabolismo
Imunoprecipitação
Retículo Endoplasmático/metabolismo
Receptores de Inositol 1,4,5-Trifosfato/metabolismo
Técnicas de Silenciamento de Genes
Proteínas de Choque Térmico/metabolismo
Camundongos Endogâmicos C57BL
Neurônios/metabolismo
Limites: Animais
Masculino
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


  4 / 20 LILACS  
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Id: biblio-950862
Autor: Han, Xu; Wang, Lingling; Ning, Yu; Li, Shuang; Wang, Zhenjun.
Título: Long non-coding RNA AFAP1-AS1 facilitates tumor growth and promotes metastasis in colorectal cancer
Fonte: Biol. Res;49:1-7, 2016. ilus, graf.
Idioma: en.
Resumo: BACKGROUND AND OBJECTIVE: Long non-coding RNAs can regulate tumorigenesis of various cancers. Dys-regulation of lncRNA-AFAP1-AS1 has not been studied in colorectal carcinoma (CRC). This study was to examine the function involvement of AFAP1-AS1 in tumor growth and metastasis of CRC. METHODS: Relative expression of AFAP1-AS1 in CRC tissues and CRC cells lines was determined using quantitative real-time PCR (qRT-PCR). Functional involvement of AFAP1-AS1 in tumor proliferation and metastasis was evaluated in AFAP1-AS1-specific siRNA-treated CRC cells and in CRC cell xenograft. Expression of epithelial-mesenchymal transition (EMT)-related gene expression was determined using western blot. RESULTS: Relative expression of AFAP1-AS1 was significantly elevated in CRC tissues and CRC HCT116 and SW480 cell lines. AFAP1-AS1 knock-down suppressed SW480 cell proliferation, colony formation, migration and invasion. Also AFAP1-AS1 knock-down inhibited tumor metastasis-associated genes expression in terms of EMT. This carcinostatic action by AFAP1-AS1 knock-down was further confirmed by suppression of tumor formation and hepatic metastasis of CRC cells in nude mice. CONCLUSION: lncRNA-AFAP1-AS1 knock-down exhibits antitumor effect on colorectal carcinoma in respects of suppression of cell proliferation and metastasis of cancer cells.
Descritores: Carcinoma/secundário
Neoplasias Colorretais/patologia
RNA Longo não Codificante/metabolismo
Neoplasias Hepáticas/secundário
-Células Tumorais Cultivadas
Carcinoma/genética
Carcinoma/metabolismo
Carcinoma/patologia
Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Regulação Neoplásica da Expressão Gênica
Movimento Celular
Western Blotting
Células HCT116
Proliferação de Células
Técnicas de Silenciamento de Genes
Transição Epitelial-Mesenquimal
Reação em Cadeia da Polimerase em Tempo Real
RNA Longo não Codificante/análise
Neoplasias Hepáticas/genética
Camundongos Endogâmicos C57BL
Camundongos Nus
Limites: Humanos
Animais
Masculino
Responsável: CL1.1 - Biblioteca Central


  5 / 20 LILACS  
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Id: biblio-950878
Autor: Zhang, Xia; Li, Yuehua; Wang, Dan; Wei, Xiaoer.
Título: miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1
Fonte: Biol. Res;50:27, 2017. graf.
Idioma: en.
Projeto: Shanghai Municipal Natural Science Foundation.
Resumo: BACKGROUND: miR-22 has been shown to be frequently downregulated and act as a tumor suppressor in multiple cancers including breast cancers. However, the role of miR-22 in regulating the radioresistance of breast cancer cells, as well as its underlying mechanism is still not well understood. METHODS: The expressions of miR-22 and sirt1 at mRNA and protein levels were examined by qRT-PCR and Western Blot. The effects of miR-22 overexpression and sirt1 knockdown on cell viability, apoptosis, radiosensitivity, γ-H2AX foci formation were evaluated by CCK-8 assay, flow cytometry, colony formation assay, and γ-H2AX foci formation assay, respectively. Luciferase reporter assay and qRT-PCR analysis were performed to confirm the interaction between miR-22 and sirt1. RESULTS: miR-22 was downregulated and sirt1 was upregulated at both mRNA and protein levels in breast cancer cells. miR-22 overexpression or sirt1 knockdown significantly suppressed viability, induced apoptosis, reduced survival fraction, and increased the number of γ-H2AX foci in breast cancer cells. Sirt1 was identified as a target of miR-22 and miR-22 negatively regulated sirt1 expression. Ectopic expression of sirt1 dramatically reversed the inhibitory effect of miR-22 on cell viability and promotive effect on apoptotic rates and radiosensitivity in breast cancer cells. CONCLUSIONS: miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting sirt1, providing a promising therapeutic target for breast cancer.
Descritores: Tolerância a Radiação
Neoplasias da Mama/radioterapia
MicroRNAs/metabolismo
Sirtuína 1/metabolismo
-Dosagem Radioterapêutica
Neoplasias da Mama/metabolismo
Histonas/metabolismo
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
Sobrevivência Celular
Apoptose/genética
Linhagem Celular Tumoral
Técnicas de Silenciamento de Genes
Sirtuína 1/genética
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central


  6 / 20 LILACS  
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Id: biblio-950907
Autor: Meng, Minjun; Chen, Yanling; Jia, Jianbo; Li, Lianghui; Yang, Sumei.
Título: Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell lines
Fonte: Biol. Res;51:24, 2018. tab, graf.
Idioma: en.
Resumo: BACKGROUND: Phosphoribosylaminoimidazole carboxylase, phosphoribosylaminoimidazole succinocarboxamide synthetase (PAICS), an enzyme required for de novo purine biosynthesis, is associated with and involved in tumorigenesis. This study aimed to evaluate the role of PAICS in human breast cancer, which remains the most frequently diagnosed cancer and the leading cause of cancer-related death among women in less developed countries. RESULTS: Lentivirus-based short hairpin RNA targeting PAICS specifically depleted its endogenous expression in ZR-75-30 and MDA-MB-231 breast cancer cells. Depletion of PAICS led to a significant decrease in cell viability and proliferation. To ascertain the mechanisms through which PAICS modulates cell proliferation, flow cytometry was performed, and it was confirmed that G1-S transition was blocked in ZR-75-30 cells through PAICS knockdown. This might have occurred partly through the suppression of Cyclin E and the upregulation of Cyclin D1, P21, and CDK4. Moreover, PAICS knockdown obviously promoted cell apoptosis in ZR-75-30 cells through the activation of PARP and caspase 3 and downregulation of Bcl-2 and Bcl-xl expression in ZR-75-30 cells. CONCLUSIONS: These findings demonstrate that PAICS plays an essential role in breast cancer proliferation in vitro, which provides a new opportunity for discovering and identifying novel effective treatment strategies.
Descritores: Peptídeo Sintases/fisiologia
Neoplasias da Mama/enzimologia
Neoplasias da Mama/patologia
Carboxiliases/biossíntese
Biomarcadores Tumorais/fisiologia
Proliferação de Células
-Peptídeo Sintases/genética
Regulação Enzimológica da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Linhagem Celular Tumoral
Técnicas de Silenciamento de Genes
Citometria de Fluxo
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central


  7 / 20 LILACS  
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Id: biblio-983941
Autor: Wu, Milu; Fan, Baohua; Guo, Qijing; Li, Yan; Chen, Rong; Lv, Nannan; Diao, Yinzhuo; Luo, Yushuang.
Título: Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation
Fonte: Biol. Res;51:39, 2018. graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . Scientific Research Project Funds of Qinghai Department.
Resumo: BACKGROUND: SET domain bifurcated 1 (SETDB1) has been widely considered as an oncogene playing a critical role in many human cancers, including breast cancer. Nevertheless, the molecular mechanism by which SETDB1 regulates breast cancer tumorigenesis is still unknown. METHODS: qRT-PCR assay or western blot analysis was performed to assess the expression level of SETDB1 mRNA or protein, respectively. siSETDB1, pCMV6-XL5-SETDB1, miR-381-3p mimic, or miR-381-3p inhibitor was transfected into cells to regulate the expression of SETDB1 or miR-381-3p. MiRNA directly interacted with SETDB1 was verified by luciferase reporter assay and RNA immunoprecipitation. CCK-8 assay, colony formation assay, flow cytometric analysis, and transwell assay were used to detect the abilities of cell proliferation, cell cycle progression and migration, respectively. Animal model of xenograft tumor was used to observe the regulatory effect of SETDB1 on tumor growth in vivo. RESULTS: We verified that SETDB1 mRNA level was upregulated in breast cancer tissues and cell lines, and SETDB1 depletion led to a suppression of cell proliferation, cell cycle progression and migration in vitro, as well as tumor growth in vivo. SETDB1 was verified to be a target of miR-381-3p. Moreover, miR-381-3p overexpression suppressed cell proliferation, cell cycle progression and migration, whereas SETDB1 abated miR-381-3p-mediated regulatory function on breast cancer cells. CONCLUSIONS: This study revealed that SETDB1 knockdown might suppress breast cancer progression at least partly by miR-381-3p-related regulation, providing a novel prospect in breast cancer therapy.
Descritores: Proteínas Metiltransferases/genética
Neoplasias da Mama/genética
MicroRNAs/metabolismo
-Proteínas Metiltransferases/metabolismo
Células-Tronco
Neoplasias da Mama/patologia
Histona-Lisina N-Metiltransferase
Reação em Cadeia da Polimerase Via Transcriptase Reversa
MicroRNAs/genética
Linhagem Celular Tumoral
Proliferação de Células
Modelos Animais de Doenças
Técnicas de Silenciamento de Genes
Citometria de Fluxo
Camundongos Endogâmicos BALB C
Limites: Humanos
Animais
Masculino
Feminino
Camundongos
Responsável: CL1.1 - Biblioteca Central


  8 / 20 LILACS  
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Id: biblio-1011402
Autor: Wang, Yanqiu; Xiang, Jun; Wang, Jianjun; Ji, Yazhong.
Título: Downregulation of TGF-ß1 suppressed proliferation and increased chemosensitivity of ovarian cancer cells by promoting BRCA1/Smad3 signaling
Fonte: Biol. Res;51:58, 2018. graf.
Idioma: en.
Projeto: National Natural Science Fund of China; . Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases.
Resumo: BACKGROUND: Studies have demonstrated that transforming growth factor beta-1 (TGF-ß1) exhibits oncogenic activity in different types of cancer, including ovarian cancer (OC). However, its regulatory mechanism in OC and whether TGF-ß1 is involved in chemosensitivity regulation remains unclear. Thus, the aim of this study was to investigate the role of TGF-ß1 in OC. METHODS: The OC cell line SKOV3 was employed, and TGF-ß1 overexpression or knockdown vectors were constructed. The cell proliferation of SKOV3 was evaluated with the cell counting kit (CCK8) kit after treatment with different concentrations of cis-platinum. Western blot and protein immunoprecipitation were employed to detect changes in BRCA1 and Smad3 expression and their interactions. Tumor growth in nude mice was evaluated. RESULTS: The results showed that TGF-ß1 knockdown increased chemosensitivity by promoting BRCA1 expression and Smad3 phosphorylation. In vivo studies showed that TGF-ß1 knockdown significantly inhibited the growth of tumors, also by upregulating BRCA1 expression and Smad3 phosphorylation. CONCLUSION: Taken together, our results suggest that TGF-ß1 knockdown inhibits tumor growth and increases chemosensitivity by promotion of BRCA1/Smad3 signaling.
Descritores: Neoplasias Ovarianas/metabolismo
Regulação para Baixo/fisiologia
Genes BRCA1/fisiologia
Proteína Smad3/fisiologia
Fator de Crescimento Transformador beta1/fisiologia
-Neoplasias Ovarianas/patologia
Neoplasias Ovarianas/tratamento farmacológico
Imuno-Histoquímica
Células Cultivadas
Western Blotting
Resistencia a Medicamentos Antineoplásicos/fisiologia
Proteínas Supressoras de Tumor/fisiologia
Linhagem Celular Tumoral
Proliferação de Células
Proteína Smad3/análise
Fator de Crescimento Transformador beta1/análise
Técnicas de Silenciamento de Genes
Reação em Cadeia da Polimerase em Tempo Real
Camundongos Endogâmicos BALB C
Limites: Humanos
Animais
Masculino
Feminino
Responsável: CL1.1 - Biblioteca Central


  9 / 20 LILACS  
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Id: biblio-881898
Autor: Knebel, Franciele Hinterholz.
Título: Amilóide Sérica A (SAA) e câncer: efeitos biológicos e mecanismos de ação em glioblastomas multiformes / Serum amyloid A (SAA) and cancer: biological effects and mechanisms of action in glioblastomas multiformes.
Fonte: São Paulo; s.n; 2014. 158 p. ilus, graf, tab.
Idioma: pt.
Tese: Apresentada a Universidade de São Paulo. Faculdade de Ciências Farmacêuticas para obtenção do grau de Doutor.
Resumo: Células tumorais têm sua proliferação e mobilidade modificada por diversos fatores de crescimento, citocinas e mediadores inflamatórios, dentre os quais a amilóide sérica A (SAA). Estudos prévios do nosso grupo mostraram o efeito direto da SAA em processos de proliferação, migração e invasão de células de glioblastoma multiforme (GBM), A172 e T98G. Neste estudo nós complementamos resultados prévios de migração e invasão; avaliamos SAA como possível indutora de moléculas importantes para a invasividade do tumor, como as MMP-2 e -9 e ROS; realizamos ensaio clonogênico com a intenção de investigar uma possível contribuição da rSAA no estágio inicial de desenvolvimento do tumor; avaliamos o impacto da hipóxia na expressão dos diferente genes da SAA; estimulamos as células com indutores hepáticos clássicos da SAA e analisamos a possibilidade destes induzirem os diferentes genes da SAA em células tumorais; avaliamos possíveis receptores e vias de sinalizações envolvidas nos processos de proliferação, migração e invasão. Construímos knockdowns (KDs) dos genes da SAA de fase aguda (SAA1 e 2) e constitutiva (SAA4) e avaliamos a função de cada um deles para a morfologia e para os processos de proliferação, migração e invasão de GBM. Por fim investigamos SAA como possível biomarcadora de gliomas em amostras clínicas. Nossos resultados sugerem que rSAA afetou a atividade das MMP-2 e -9 e a produção de ROS em ambos GBM, mas não se mostrou clonogênica. As citocinas IL-6, TNF-α e IL-1ß, mas não a hipóxia, foram capazes de induzir os diferentes genes da SAA. A adição de rSAA às culturas celulares estimulou a transrição dos diferentes genes da SAA, sugerindo a ativação de mecanismos intracelulares retroalimentados. Efeitos pró-tumorais da rSAA parecem ser viabilizados via RAGE, enquanto efeitos anti-tumorais parecem ser induzidos via TLR-4. Pela primeira vez mostramos que SAA induz aumento de RAGE. KDs da SAA inibiram proliferação, migração e invasão, sugerindo que SAA seja um produto tumoral importante para a manutenção do fenótipo invasivo de GBM. A adição de SAA exógena reverteu grande parte dos efeitos nas células T98G KD, enquanto células A172 KD responderam parcialmente à rSAA. KDs da SAA sugerem a mesma como mantenedora da morfologia das células de GBM. De maneira inédita mostramos que o gene SAA4 até então descrito como um gene constitutivo de função desconhecida é importante para a proliferação, migração e invasão de GBM. Nós especulamos que os efeitos diferenciados induzidos por rSAA nos GBM estejam associados à natureza multiligante da SAA e às diferenças genéticas dos GBM. Pacientes com GBM apresentaram aumento significativo na transcrição e expressão de SAA1 no tecido tumoral, bem como aumento sérico de SAA. A correlação na expressão de SAA1 com moléculas importantes para progressão tumoral, como CXCR4, CXCR7, CD163 e HIF-1α também a identificam como uma proteína associada à malignidade

Tumor cells have their proliferation and migration modified by several growth factors, cytokines and inflammatory mediators, such as serum amyloid A (SAA). Previous studies from our group showed the direct effect of SAA on proliferation, migration and invasion of glioblastoma multiforme (GBM) cells, A172 and T98G. In this study we complemented previous migration and invasion data; evaluated SAA as possible inducer of MMP-2, -9 and ROS; performed clonogenic assay to investigate a possible contribution of rSAA in the early stage of tumor development; evaluated the impact of hypoxia on the expression of different genes of SAA; stimulated the cells with classics inducers of hepatic SAA and analyzed the possibility of these different genes to induce SAA in tumor cells; evaluated possible receptors and signaling pathways involved in proliferation, migration and invasion processes. SAA knockdowns (KDs) were made for acute phase (SAA1 and 2) and constitutive protein (SAA4) and evaluated their role in cell proliferation, migration, morfology and invasion. Finally it was investigated SAA as a possible biomarker of glioma grade in clinical samples. Our results suggest that rSAA affects MMP-2 and -9 activity and ROS production in both GBM, but did not affect clonogenicity. IL-6, TNF-α and IL-1ß, but not hypoxia, were able to induce SAA expression. rSAA addition to cell cultures stimulated transcription of the three different SAA genes, suggesting the activation of intracellular feedback mechanisms. Pro-tumor effects of rSAA seem to occur via RAGE and anti-tumor effects appear to be induced via TLR-4. This was de first time that induction of RAGE triggered by rSAA was shown. Proliferation, migration and invasion were inhibited in SAA KDs, suggesting that SAA is an important tumoral product for the maintenance of the invasive phenotype of GBM. The addition of exogenous SAA largely reversed the effects on SAA KDs T98G cells, whereas SAA KDs A172 cells partially responded to the rSAA. The findings with SAA KDs suggest that SAA affect cell morphology. Another new contribution from our study was that SAA4, a constitutive gene with unknown function, was important for the proliferation, migration and invasion of GBM and it can be induced by rSAA, IL-6, TNF-α and IL-1ß. We speculate that the different effects induced by rSAA in GBM are associated with the affinity of SAA to different receptors and the different genetic backgrounds of GBM. Patients with GBM showed a significant increase in the transcription and expression of SAA1 in tumor tissue as well as increased serum SAA. The correlation between the expression of SAA1 with important molecules for tumor progression, such as CXCR4, CXCR7, CD163 and HIF-1α also identified SAA as a protein associated with malignancy
Descritores: Glioblastoma/metabolismo
Proteína Amiloide A Sérica/análise
-Hipóxia Celular
Movimento Celular
Proliferação de Células
Ensaio de Unidades Formadoras de Colônias/estatística & dados numéricos
Técnicas de Silenciamento de Genes/métodos
Ensaio Tumoral de Célula-Tronco/métodos
Tipo de Publ: Revisão
Responsável: BR40.1 - DBD - Divisão de Biblioteca e Documentacão do Conjunto das Químicas
BR40.1; T 616.0756, K68am. 30100021778-F


  10 / 20 LILACS  
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Id: biblio-853665
Autor: Chiconelli, Caroline Papi Crespo; Curitiba; Curitiba; Curitiba.
Título: Prevalence of Pain after Endodontic Treatment
Fonte: Pesqui. bras. odontopediatria clín. integr;14(3):249-257, jul. 2014. tab.
Idioma: en.
Resumo: Objective:To evaluate the prevalence of postoperative pain and its intensity in association with clinical factors in patients undergoing root canal treatment. Material and Methods:50 subjects over 18 years of age of both genders were included by demand. Questionnaires were applied to subjects in order to obtain demographic data, clinical features about presence of pain and its intensity at intervals of 24 and 48 hours after procedure. Teeth were treated by the crown-down technique in single or multiple visits, aided by irrigation with 2.5% sodium hypochlorite, proceeding to the filling of root canals by the Tagger's hybrid technique, using gutta-percha and zinc oxide-eugenol cement. Data were analyzed with univariate and bivariate statistical test (Fisher's exact test) using SPSS 13.0 software. Results:No statistical difference (p>0.05) was observed between prevalence of postoperative pain and its magnitude in association with clinical variables. Conclusion:Pulp sensitivity (vitality), pre-existence of apical lesion, single-session treatment, use of intracanal dressing, reported pain prior to treatment, and use of analgesic medication were not associated with the prevalence of postoperative pain
Descritores: Dor
Prevalência
Sensibilidade da Dentina/diagnóstico
Técnicas de Silenciamento de Genes/métodos
Tratamento do Canal Radicular/métodos
-Brasil
Equipamentos Odontológicos de Alta Rotação
Inquéritos e Questionários
Instrumentos Odontológicos
Radiografia Dentária/instrumentação
Limites: Humanos
Masculino
Feminino
Adulto Jovem
Adulto
Pessoa de Meia-Idade
Idoso
Responsável: BR1264.1 - Biblioteca Setorial Prof Alberto M Campos



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