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Pesquisa : G05.308.370 [Categoria DeCS]
Referências encontradas : 136 [refinar]
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Id: biblio-1019500
Autor: Do, Hyunhee; Kim, Dain; Kang, JiHoon; Son, Beomseok; Seo, Danbi; Youn, HyeSook; Youn, BuHyun; Kim, Wanyeon.
Título: TFAP2C increases cell proliferation by downregulating GADD45B and PMAIP1 in non-small cell lung cancer cells
Fonte: Biol. Res;52:35, 2019. tab, graf.
Idioma: en.
Projeto: Ministry of Education; . Ministry of Science; . ICT.
Resumo: BACKGROUND: Non-small cell lung cancer (NSCLC) is one of the leading causes of death in the world. NSCLC diagnosed at an early stage can be highly curable with a positive prognosis, but biomarker limitations make it difficult to diagnose lung cancer at an early stage. To identify biomarkers for lung cancer development, we previously focused on the oncogenic roles of transcription factor TFAP2C in lung cancers and revealed the molecular mechanism of several oncogenes in lung tumorigenesis based on TFAP2C-related microarray analysis. RESULTS: In this study, we analyzed microarray data to identify tumor suppressor genes and nine genes downregulated by TFAP2C were screened. Among the nine genes, we focused on growth arrest and DNA-damage-inducible beta (GADD45B) and phorbol-12-myristate-13-acetate-induced protein 1 (PMAIP1) as representative TFAP2C-regulated tumor suppressor genes. It was observed that overexpressed TFAP2C resulted in inhibition of GADD45B and PMAIP1 expressions at both the mRNA and protein levels in NSCLC cells. In addition, downregulation of GADD45B and PMAIP1 by TFAP2C promoted cell proliferation and cell motility, which are closely associated with NSCLC tumorigenesis. CONCLUSION: This study indicates that GADD45B and PMAIP1 could be promising tumor suppressors for NSCLC and might be useful as prognostic markers for use in NSCLC therapy.
Descritores: Antígenos de Diferenciação/genética
Regulação para Baixo/genética
Carcinoma Pulmonar de Células não Pequenas/genética
Proliferação de Células/genética
Fator de Transcrição AP-2/genética
Neoplasias Pulmonares/genética
-RNA Mensageiro/análise
Biomarcadores Tumorais/análise
Regulação Neoplásica da Expressão Gênica
Genes Supressores de Tumor/fisiologia
RNA Interferente Pequeno/análise
Linhagem Celular Tumoral
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1019506
Autor: Li, Wei; Chen, Yan; Sun, Xuan; Yang, Jupeng; Zhang, David Y; Wang, Daguang; Suo, Jian.
Título: Protein expression profiles and clinicopathologic characteristics associate with gastric cancer survival
Fonte: Biol. Res;52:42, 2019. tab, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . Excellent Young Foundation of Jilin Scientific and Technological Development Program.
Resumo: BACKGROUND: Prognosis remains one of most crucial determinants of gastric cancer (GC) treatment, but current methods do not predict prognosis accurately. Identification of additional biomarkers is urgently required to identify patients at risk of poor prognoses. METHODS: Tissue microarrays were used to measure expression of nine GC-associated proteins in GC tissue and normal gastric tissue samples. Hierarchical cluster analysis of microarray data and feature selection for factors associated with survival were performed. Based on these data, prognostic scoring models were established to predict clinical outcomes. Finally, ingenuity pathway analysis (IPA) was used to identify a biological GC network. RESULTS: Eight proteins were upregulated in GC tissues versus normal gastric tissues. Hierarchical cluster analysis and feature selection showed that overall survival was worse in cyclin dependent kinase (CDK)2, Akt1, X-linked inhibitor of apoptosis protein (XIAP), Notch4, and phosphorylated (p)-protein kinase C (PKC) α/ß2 immunopositive patients than in patients that were immunonegative for these proteins. Risk score models based on these five proteins and clinicopathological characteristics were established to determine prognoses of GC patients. These proteins were found to be involved in cancer related-signaling pathways and upstream regulators were identified. CONCLUSION: This study identified proteins that can be used as clinical biomarkers and established a risk score model based on these proteins and clinicopathological characteristics to assess GC prognosis.
Descritores: Neoplasias Gástricas/mortalidade
Biomarcadores Tumorais/metabolismo
Proteínas de Neoplasias/metabolismo
-Prognóstico
Neoplasias Gástricas/metabolismo
Neoplasias Gástricas/patologia
Imuno-Histoquímica
Regulação Neoplásica da Expressão Gênica
Análise de Sobrevida
Análise Serial de Tecidos
Estadiamento de Neoplasias
Limites: Humanos
Masculino
Feminino
Pessoa de Meia-Idade
Idoso
Responsável: CL1.1 - Biblioteca Central


  3 / 136 LILACS  
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Id: biblio-1100916
Autor: Li, Yan; Zhou, Jinhua; Wang, Juan; Chen, Xiaoping; Zhu, Yan; Chen, Youguo.
Título: Mir-30b-3p affects the migration and invasion function of ovarian cancer cells by targeting the CTHRC1 gene
Fonte: Biol. Res;53:10, 2020. tab, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . Jiangsu Provincial Medical Youth Talent; . Jiangsu Provincial Maternal and Child Health Association.
Resumo: BACKGROUND: The aim of this study was to investigate the effect role and mechanism of miR-30b-3p on ovarian cancer cells biological function. METHODS: The expression of miR-30b-3p was detected in ovarian cancer cell lines and normal ovarian epithelial cell line by qRT-PCR. Mir-30b-3p mimic was transfected into OVCAR3 cells. Cell-counting kit-8 (CCK-8) assay was conducted to explore the effect of mir-30b-3p on the OVCAR3 cells' proliferation. Cell cycle and apoptosis were detected by Flow cytometry. Cell invasion ability was detected by Transwell test. The regulation of putative target of miR-30b-3p was verified by double luciferase reporter assays and Western blot. RESULT: We found that miR-30b-3p was downregulated in OVCAR3 cells. Overexpression of miR-30b-3p suppressed proliferation, promoted apoptosis, slowed cell cycle and inhibited migration and invasion of OVCAR3 cells. Bioinformatics analysis identified 3'-untranslated region (3'UTR) of Collagen triple helix repeat-containing 1 (CTHRC1) as the presumed binding site for miR-30b-3p. Detection of double luciferase reporter and Western-Blot result confirmed that CTHRC1 was the target gene of miR-30b-3p. Furthermore, E-cadherin, ß-cadherin and Vimentin protein expression level were changed after transfection of miR-30b-3p. CONCLUSION: miR-30b-3p function as an anti-cancer gene. Overexpression of miR-30b-3p can inhibit the biological function of ovarian cancer cells. MiR-30b-3p targets CTHRC1 gene plays an important role in epithelial-mesenchymal transformation (EMT), and supports miR-30b-3p as a potential biological indicator for ovarian cancer in the future.
Descritores: Neoplasias Ovarianas/genética
Regulação Neoplásica da Expressão Gênica/genética
Proteínas da Matriz Extracelular/genética
MicroRNAs/genética
Transição Epitelial-Mesenquimal/genética
-Neoplasias Ovarianas/metabolismo
Transdução de Sinais
Movimento Celular
Proteínas da Matriz Extracelular/metabolismo
Apoptose
Linhagem Celular Tumoral
Proliferação de Células
Invasividade Neoplásica
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central


  4 / 136 LILACS  
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Id: biblio-1100917
Autor: Zhao, Guizhi; Wei, Zhili; Guo, Yang.
Título: MicroRNA-107 is a novel tumor suppressor targeting POU3F2 in melanoma
Fonte: Biol. Res;53:11, 2020. graf.
Idioma: en.
Resumo: BACKGROUND: Melanoma is one of the major types of skin cancer. The metastatic melanoma is among the most lethal forms of malignant skin tumors. We hereby aimed to characterize a novel microRNA (miR) in the metastatic melanoma model. METHODS: First, we evaluated the expression of miR-107 in melanoma cells and tumor tissues. The comparison between primary and metastatic cancer tissues was also accessed. Next, we examined the impact of miR-107 on melanoma cell proliferation, cell cycle, colony formation, apoptotic activity, migration and matrix invasion. A downstream target of miR-107 was also predicted and validated functionally in melanoma cells. RESULTS: Our findings showed miR-107 was significantly downregulated in melanoma. Its expression was lowest in metastatic form. Over-expression of miR-107 reduced melanoma cell proliferation, migration and invasion. POU3F2 was identified as the downstream target of miR-107. Over-expression of POU3F2 antagonized miR-107-mediated inhibitory effect on melanoma cells. CONCLUSION: Our study has reported miR-107 as a novel tumor suppressive factor in the metastatic melanoma model. It has provided new avenue to manage melanoma and improve the survival rate in the advanced stage.
Descritores: Regulação Neoplásica da Expressão Gênica
Genes Supressores de Tumor
MicroRNAs/genética
Fatores do Domínio POU/genética
Melanoma/genética
-Ensaio Tumoral de Célula-Tronco
Movimento Celular
Linhagem Celular Tumoral
Proliferação de Células
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1100920
Autor: Luo, Min; Liang, Chengbai.
Título: LncRNA LINC00483 promotes gastric cancer development through regulating MAPK1 expression by sponging miR-490-3p
Fonte: Biol. Res;53:14, 2020. graf.
Idioma: en.
Resumo: BACKGROUND: Previous studies have shown that long noncoding RNA (IncRNA) LINC00483 was aberrantly expressed in human cancers, including gastric cancer. However, the regulatory mechanism of this IncRNA in gastric cancer remains largely unknown. The present study aimed to investigate the effect of LINC00483 on gastric cancer development and explore the potential regulatory network of LINC00483/microRNA (miR)-490-3p/mitogen-activated protein kinase 1 (MAPK1). METHODS: Thirty patients with gastric cancer were recruited for tissues collection. The expression levels of LINC00483, miR-490-3p and MAPK1 were detected by quantitative real-time polymerase chain reaction or western blot. Cell viability, apoptosis, migration and invasion were determined by MTT, flow cytometry, transwell assays and western blot, respectively. The target association between miR-490-3p and LINC00483 or MAPK1 was confirmed by luciferase reporter assay. Xenograft model was established to assess the function of LINC00483 in vivo. RESULTS: LINC00483 and MAPK1 levels were increased in gastric cancer tissues and cells. Knockdown of LINC00483 or MAPK1 inhibited cells viability, migration and invasion but promoted apoptosis in gastric cancer cells. Moreover, MAPK1 overexpression attenuated the effect of LINC00483 knockdown on gastric cancer development. LINC00483 could increase MAPK1 expression by competitively sponging miR-490-3p. miR-490-3p overexpression suppressed gastric cancer development, which was abated by introduction of LINC00483. Besides, inhibition of LINC00483 decreased xenograft tumor growth by regulating miR-490-3p/MAPK1 axis. CONCLUSION: Knockdown of LINC00483 inhibited gastric cancer development in vitro and in vivo by increasing miR- 490-3p and decreasing MAPK1, elucidating a novel mechanism for understanding the development of gastric cancer.
Descritores: Neoplasias Gástricas/metabolismo
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
MicroRNAs/metabolismo
RNA Longo não Codificante/metabolismo
-Neoplasias Gástricas/genética
Regulação Neoplásica da Expressão Gênica
Movimento Celular
Sobrevivência Celular
Apoptose
Ensaios Antitumorais Modelo de Xenoenxerto
MicroRNAs/genética
Linhagem Celular Tumoral/metabolismo
Células Epiteliais/metabolismo
RNA Longo não Codificante/genética
Carcinogênese/metabolismo
Luciferases/metabolismo
Camundongos Endogâmicos BALB C
Limites: Humanos
Animais
Masculino
Responsável: CL1.1 - Biblioteca Central


  6 / 136 LILACS  
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Id: biblio-1124204
Autor: Zhang, Yun; Ai, Hao; Fan, Xue; Chen, Suxian; Wang, Yadi; Liu, Lili.
Título: Knockdown of long non-coding RNA HOTAIR reverses cisplatin resistance of ovarian cancer cells through inhibiting miR-138-5p-regulated EZH2 and SIRT1
Fonte: Biol. Res;53:18, 2020. tab, graf.
Idioma: en.
Projeto: Natural Science Foundation of Liaoning Province.
Resumo: BACKGROUND: Cisplatin resistance (DDP-resistance) remains one of the major causes of poor prognosis in females with ovarian cancer. Long non-coding RNAs (lncRNAs) have been shown to participate in the regulation of cellular processes, including chemoresistance. The aim of this study was to explore the role of HOX transcript antisense RNA (HOTAIR) in DDP-resistant ovarian cancer cells. METHODS: DDP-resistant ovarian cancer cell lines (SKOV3/DDP and A2780/DDP) were established. Real-time PCR, western blot, dual-luciferase reporter assay, and flow cytometry were then used to evaluate the effect of HOTAIR/miR-138-5p axis on chemoresistance of DDP-resistant ovarian cancer cells to DDP. RESULTS: We found that HOTAIR was upregulated in DDP-resistant cells, while miR-138-5p was downregulated. Knockdown of HOTAIR increased the expression of miR-138-5p in DDP-resistant cells and miR-138-5p is directly bound to HOTAIR. Upregulation of miR-138-5p induced by HOTAIR siRNA or by its mimics enhanced the chemosensitivity of DDP-resistant cells and decreased the expression of EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) and SIRT1 (sirtuin 1). Furthermore, the HOTAIR silencing-induced chemosensitivity of DDP-resistant cells was weakened by miR-138-5p inhibitor. CONCLUSIONS: These data demonstrate that HOTAIR acts as a sponge of miR-138-5p to prevent its binding to EZH2 and SIRT1, thereby promoting DDP-resistance of ovarian cancer cells. Our work will shed light on the development of therapeutic strategies for ovarian cancer treatment.
Descritores: Neoplasias Ovarianas/genética
Cisplatino/farmacologia
Resistencia a Medicamentos Antineoplásicos/genética
RNA Longo não Codificante/genética
-Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Regulação para Cima
Apoptose/efeitos dos fármacos
MicroRNAs/antagonistas & inibidores
Linhagem Celular Tumoral
Técnicas de Inativação de Genes/métodos
Sirtuína 1/antagonistas & inibidores
Reação em Cadeia da Polimerase em Tempo Real
Proteína Potenciadora do Homólogo 2 de Zeste/antagonistas & inibidores
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1114696
Autor: Degerli, Elif; Torun, Vildan; Cansaran-Duman, Demet.
Título: miR-185-5p response to usnic acid suppresses proliferation and regulating apoptosis in breast cancer cell by targeting Bcl2
Fonte: Biol. Res;53:19, 2020. graf.
Idioma: en.
Projeto: Ankara University Management of Scientific Research Projects.
Resumo: BACKGROUND: Breast cancer is the most common cancer types among women. Recent researches have focused on determining the efficiency of alternative molecules and miRNAs in breast cancer treatment. The AIMof this study was to determine the effect of usnic acid response-miR-185-5p on proliferation in the breast cancer cell and to determine its relationship with apoptosis pathway. METHODS: The cell proliferation and cell apoptosis rate were significantly increased following the ectopic expression of miR-185-5p in BT-474 cells. Furthermore, the results of cell cycle assay performed by flow cytometry revealed that the transfection with miR-185-5p induced G1/S phase arrest. The apoptosis-related genes expression analysis was performed by qRT-PCR and the direct target of miR-185-5p in BT-474 cells was identified by western blot and luciferase reporter assay. RESULTS: Our data showed that miR-185-5p can cause significant changes in apoptosis-related genes expression levels, suggesting that cell proliferation was suppressed by miR-185-5p via inducing apoptosis in breast cancer cells. According to western blot results, miR-185-5p lead to decrease BCL2 protein level in BT-474 cells and direct target of miR-185-5p was identified as BCL by luciferase reporter assay. CONCLUSION: This study revealed that miR-185-5p may be an effective agent in the treatment of breast cancer.
Descritores: Benzofuranos/metabolismo
Neoplasias da Mama/genética
Proteínas Proto-Oncogênicas c-bcl-2/genética
MicroRNAs/genética
-Neoplasias da Mama/metabolismo
Transfecção
Transdução de Sinais
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
Apoptose
Proteínas Proto-Oncogênicas c-bcl-2
Reação em Cadeia da Polimerase Via Transcriptase Reversa
MicroRNAs/metabolismo
Linhagem Celular Tumoral
Proliferação de Células
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1001213
Autor: Silva, Tabata M; Moretto, Fernanda C F; Sibio, Maria T De; Gonçalves, Bianca M; Oliveira, Miriane; Olimpio, Regiane M C; Oliveira, Diego A M; Costa, Sarah M B; Deprá, Igor C; Namba, Vickeline; Nunes, Maria T; Nogueira, Célia R.
Título: Triiodothyronine (T3) upregulates the expression of proto-oncogene TGFA independent of MAPK/ERK pathway activation in the human breast adenocarcinoma cell line, MCF7
Fonte: Arch. endocrinol. metab. (Online);63(2):142-147, Mar.-Apr. 2019. graf.
Idioma: en.
Projeto: FAPESP.
Resumo: ABSTRACT Objective: To verify the physiological action of triiodothyronine T3 on the expression of transforming growth factor α (TGFA) mRNA in MCF7 cells by inhibition of RNA Polymerase II and the MAPK/ERK pathway Materials and methods: The cell line was treated with T3 at a physiological dose (10−9M) for 10 minutes, 1 and 4 hour (h) in the presence or absence of the inhibitors, α-amanitin (RNA polymerase II inhibitor) and PD98059 (MAPK/ERK pathway inhibitor). TGFA mRNA expression was analyzed by RT-PCR. For data analysis, we used ANOVA, complemented with the Tukey test and Student t-test, with a minimum significance of 5%. Results: T3 increases the expression of TGFA mRNA in MCF7 cells in 4 h of treatment. Inhibition of RNA polymerase II modulates the effect of T3 treatment on the expression of TGFA in MCF7 cells. Activation of the MAPK/ERK pathway is not required for T3 to affect the expression of TGFA mRNA. Conclusion: Treatment with a physiological concentration of T3 after RNA polymerase II inhibition altered the expression of TGFA. Inhibition of the MAPK/ERK pathway after T3 treatment does not interfere with the TGFA gene expression in a breast adenocarcinoma cell line.
Descritores: Tri-Iodotironina/genética
Neoplasias da Mama/genética
Adenocarcinoma/genética
Regulação Neoplásica da Expressão Gênica/genética
Fator de Crescimento Transformador alfa/genética
Sistema de Sinalização das MAP Quinases/genética
-Tri-Iodotironina/metabolismo
Tri-Iodotironina/farmacologia
Proto-Oncogenes/genética
Neoplasias da Mama/metabolismo
RNA Mensageiro/genética
Adenocarcinoma/metabolismo
Fator de Crescimento Transformador alfa/efeitos dos fármacos
Fator de Crescimento Transformador alfa/metabolismo
Linhagem Celular Tumoral/metabolismo
Células MCF-7/metabolismo
Limites: Humanos
Feminino
Responsável: BR1.1 - BIREME


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Id: biblio-889036
Autor: Zhang, X; Song, Y; Song, N; Zhang, L; Wang, Y; Li, D; Wang, Z; Qu, X; Liu, Y.
Título: Rankl expression predicts poor prognosis in gastric cancer patients: results from a retrospective and single-center analysis
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;51(3):e6265, 2018. tab, graf.
Idioma: en.
Projeto: National Science and Technology Major Project; . Science and Technology Plan Project; . Chinese National Foundation of National Sciences; . Liaoning BaiQianWan Talents Program.
Resumo: The receptor activator of nuclear factor κB ligand (RANKL)/RANK pathway plays an important role in the prognosis of several solid tumor types, but its role in gastric cancer prognosis has been poorly characterized. A total of 116 gastric cancer patients who underwent surgical resection were enrolled in this study. Expressions of RANKL and RANK in gastric cancer tissues were detected using immunohistochemical staining. Thirty-eight patients (33%) showed a high level of RANKL expression and 61 patients (53%) showed a high level of RANK expression. There was a positive correlation between expressions of RANKL and RANK (P=0.014, r=0.221). A high level of RANKL expression indicated shorter overall survival (OS) (P=0.008), and was associated with a higher pathological tumor/lymph node/metastasis (pTNM) stage (P=0.035), while no significant correlation was detected between RANK expression and clinicopathological parameters. RANKL also predicted poor prognosis in patients with high RANK expression (P=0.008) and Bormann's type III/IV (P=0.002). Furthermore, RANKL expression correlated with pTNM stage according to high RANK expression (P=0.009), while no significance was found in patients with low RANK expression (P=1.000). Together, our results revealed that high expression of RANKL could predict worse outcomes in gastric cancer especially combined with RANK detection, and thereby this pathway could be a useful prognostic indicator of gastric cancer.
Descritores: Neoplasias Gástricas/metabolismo
Adenocarcinoma/metabolismo
Ligante RANK/metabolismo
Proteínas de Neoplasias/metabolismo
-Prognóstico
Neoplasias Gástricas/cirurgia
Neoplasias Gástricas/mortalidade
Neoplasias Gástricas/patologia
Imuno-Histoquímica
Adenocarcinoma/cirurgia
Adenocarcinoma/mortalidade
Adenocarcinoma/patologia
Regulação Neoplásica da Expressão Gênica
China/epidemiologia
Estudos Retrospectivos
Estatísticas não Paramétricas
Gradação de Tumores
Estadiamento de Neoplasias
Limites: Humanos
Masculino
Feminino
Pessoa de Meia-Idade
Responsável: BR1.1 - BIREME


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Id: biblio-1024773
Autor: Lima, M A; Dos Santos, L; Turri, J A; Nonogaki, S; Buim, M; Lima, J F; de Jesus Viana Pinheiro, J; Osório, C A Bueno de Toledo; Soares, F A; Freitas, V M.
Título: Prognostic Value of ADAMTS Proteases and Their Substrates in Epithelial Ovarian Cancer
Fonte: Pathobiology;83(6):316-326, 2016.
Idioma: en.
Resumo: Background: ADAMTS are metalloproteases with disintegrin and thrombospondin motifs. They are secreted proteases playing a role in biological processes such as inflammation, angiogenesis, and urogenital development. ADAMTS have specific substrates, such as the proteoglycans (PG) versican, aggrecan, and brevican. Despite data indicating a role of ADAMTS in tumor invasion and metastases, effects played by these molecules in cancer progression are still controversial. In ovarian cancer, the importance of ADAMTS gene mutations was recently described and related to chemotherapy outcome. Objective: To analyze protein levels of ADAMTS-1, -4, and -5, and TIMP-3 in human ovarian cancer classified as benign, borderline, or malignant. We also assessed the expression of the ADAMTS substrates aggrecan, brevican, and versican in these neoplasms. Correlations between overall survival and protein expression were performed. Methods: Tumors were classified according to the WHO Classification of Tumors of Female Reproductive Organs. Protein and PG expression was studied by immunohistochemistry. Differences in labeling were analyzed by percent measurements of stained areas. Results: ADAMTS-1, ADAMTS-5, and its tissue inhibitor TIMP-3 are increased in borderline and malignant tumors compared to benign neoplasms. Aggrecan and versican levels were increased in malignant subtypes compared to benign ovarian cancer. Higher ADAMTS-1, TIMP-3, and versican expression was associated with a shorter overall survival. Conclusions: Comparison of protease, TIMP-3, and substrate expression showed that in malignant tumors all ADAMTS and TIMP-3 expression levels were significantly raised compared to the substrates studied.
Descritores: Neoplasias Ovarianas
Humanos
Biomarcadores Tumorais/metabolismo
Regulação Neoplásica da Expressão Gênica
Neoplasias Epiteliais e Glandulares/diagnóstico
Inibidor Tecidual de Metaloproteinase-3/metabolismo
Proteína ADAMTS1/metabolismo
Proteína ADAMTS4/metabolismo
FREUDIAN THEORY1
Responsável: BR91.2 - Centro de Documentação



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