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  1 / 75 LILACS  
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Menck, Carlos Frederico Martins
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Id: biblio-952835
Autor: Rocha, Clarissa Ribeiro Reily; Silva, Matheus Molina; Quinet, Annabel; Cabral-Neto, Januario Bispo; Menck, Carlos Frederico Martins.
Título: DNA repair pathways and cisplatin resistance: an intimate relationship
Fonte: Clinics;73(supl.1):e478s, 2018. tab, graf.
Idioma: en.
Projeto: Grants.
Resumo: The main goal of chemotherapeutic drugs is to induce massive cell death in tumors. Cisplatin is an antitumor drug widely used to treat several types of cancer. Despite its remarkable efficiency, most tumors show intrinsic or acquired drug resistance. The primary biological target of cisplatin is genomic DNA, and it causes a plethora of DNA lesions that block transcription and replication. These cisplatin-induced DNA lesions strongly induce cell death if they are not properly repaired or processed. To counteract cisplatin-induced DNA damage, cells use an intricate network of mechanisms, including DNA damage repair and translesion synthesis. In this review, we describe how cisplatin-induced DNA lesions are repaired or tolerated by cells and focus on the pivotal role of DNA repair and tolerance mechanisms in tumor resistance to cisplatin. In fact, several recent clinical findings have correlated the tumor cell status of DNA repair/translesion synthesis with patient response to cisplatin treatment. Furthermore, these mechanisms provide interesting targets for pharmacological modulation that can increase the efficiency of cisplatin chemotherapy.
Descritores: Dano ao DNA/genética
Cisplatino/uso terapêutico
Resistencia a Medicamentos Antineoplásicos/genética
Reparo do DNA/genética
Antineoplásicos/uso terapêutico
-Dano ao DNA/efeitos dos fármacos
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: biblio-1090612
Autor: Azambuja, Alan A; Engroff, Paula; Silva, Bruna T; Zorzetti, Roberta C. S; Morrone, Fernanda B.
Título: Evaluation of nuclear NF-κB, transglutaminase2, and ERCC1 as predictors of platinum resistance in testicular tumors
Fonte: Int. braz. j. urol;46(3):353-362, May-June 2020. tab, graf.
Idioma: en.
Resumo: ABSTRACT Purpose: Testicular germ cells tumor (TGCT) are associated with a high cure rate and are treated with platinum-based chemotherapy. However, a group of testicular cancer patients may have a very unfavorable evolution and insensitivity to the main therapeutic agent chemotherapy (CT) cisplatin. The aim of this study was to evaluate the risk of recurrence and overall survival related to the expression of nuclear factor kappa-B (NF-κB), transglutaminase 2 (TG2) and excision repair cross-complementation group 1 (ERCC1) in patients with TGCT treated with platinum combinations. Patients and Methods: A retrospective study was performed with TGCT patients treated with platinum-based chemotherapy. Immunohistochemical analysis was performed and the expression was correlated with clinical and laboratory data. Results: Fifty patients were included, the mean age was 28.4 years (18 to 45), and 76% were non-seminoma. All patients were treated with standard cisplatin, etoposide and bleomycin or cisplatin, and etoposide. Patient's analyzed immunodetection for NF-κB, TG2, and ERCC1 were positive in 76%, 54% and 42%, respectively. Multivariate analysis identified that positive expressions to ERCC1 and NF-κB are independent risk factors for higher recurrence TGCT after chemotherapy (RR 2.96 and 3.16, respectively). Patients with positive expression of ERCC1 presented a poor overall survival rate for 10-year follow (p=0.001). Conclusions: The expression of ERCC1 and NF-κB give a worse prognosis for relapse, and only ERCC1 had an influence on the overall survival of TGCT patients treated with platinum-based chemotherapy. These may represent markers that predict poor clinical outcome and response to cisplatin.
Descritores: Neoplasias Testiculares
Transglutaminases/metabolismo
NF-kappa B/metabolismo
Proteínas de Ligação ao GTP/metabolismo
Neoplasias Pulmonares
-Prognóstico
Protocolos de Quimioterapia Combinada Antineoplásica
Estudos Retrospectivos
Cisplatino
Resistencia a Medicamentos Antineoplásicos/fisiologia
Proteínas de Ligação a DNA
Reparo do DNA
Endonucleases
Limites: Humanos
Masculino
Adulto
Responsável: BR1.1 - BIREME


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Id: biblio-950723
Autor: Rosas, Carlos; Sinning, Mariana; Ferreira, Arturo; Fuenzalida, Marcela; Lemus, David.
Título: Celecoxib decreases growth and angiogenesis and promotes apoptosis in a tumor cell line resistant to chemotherapy
Fonte: Biol. Res;47:1-9, 2014. ilus, graf.
Idioma: en.
Projeto: Fondo Nacional de Desarrollo Científico y Tecnológico, Chile.
Resumo: BACKGROUND: During the last few years it has been shown in several laboratories that Celecoxib (Cx), a non-steroidal anti-inflammatory agent (NSAID) normally used for pain and arthritis, mediates antitumor and antiangiogenic effects. However, the effects of this drug on a tumor cell line resistant to chemotherapeutical drugs used in cancer have not been described. Herein we evaluate the angiogenic and antitumor effects of Cx in the development of a drug-resistant mammary adenocarcinoma tumor (TA3-MTXR). RESULTS: Cx reduces angiogenesis in the chick embryonic chorioallantoic membrane assay (CAM), inhibits the growth and microvascular density of the murine TA3-MTXR tumor, reduces microvascular density of tumor metastases, promotes apoptosis and reduces vascular endothelial growth factor (VEGF) production and cell proliferation in the tumor. CONCLUSION: The antiangiogenic and antitumor Cx effects correlate with its activity on other tumor cell lines, suggesting that Prostaglandins (PGs) and VEGF production are involved. These results open the possibility of using Celecoxib combined with other experimental therapies, ideally aiming to get synergic effects.
Descritores: Pirazóis/farmacologia
Sulfonamidas/farmacologia
Neoplasias da Mama/tratamento farmacológico
Anti-Inflamatórios não Esteroides/farmacologia
Apoptose/efeitos dos fármacos
Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos
Neoplasias Pulmonares/secundário
Neovascularização Patológica/tratamento farmacológico
-Pirazóis/administração & dosagem
Sulfonamidas/administração & dosagem
Neoplasias da Mama/patologia
Ensaios de Seleção de Medicamentos Antitumorais
Galinhas
Marcação In Situ das Extremidades Cortadas
Inibidores da Angiogênese/farmacologia
Linhagem Celular Tumoral
Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores
Membrana Corioalantoide
Proliferação de Células/efeitos dos fármacos
Celecoxib
Limites: Animais
Feminino
Embrião de Galinha
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950762
Autor: Fulawka, Lukasz; Donizy, Piotr; Halon, Agnieszka.
Título: Cancer stem cells - the current status of an old concept: literature review and clinical approaches
Fonte: Biol. Res;47:1-9, 2014. ilus.
Idioma: en.
Resumo: As regards their morphology and biology, tumours consist of heterogeneous cell populations. The cancer stem cell (CSC) hypothesis assumes that a tumour is hierarchically organized and not all of the cells are equally capable of generating descendants, similarly to normal tissue. The only cells being able to self-renew and produce a heterogeneous tumour cell population are cancer stem cells. CSCs probably derive from normal stem cells, although progenitor cells may be taken into consideration as the source of cancer stem cells. CSCs reside in the niche defined as the microenvironment formed by stromal cells, vasculature and extracellular matrix. The CSC assays include FACS sorting, xenotransplantation to immunodeficient mice (SCID), incubation with Hoechst 33342 dye, cell culture in non-adherent conditions, cell culture with bromodeoxyuridine. CSCs have certain properties that make them resistant to anticancer therapy, which suggests they may be the target for potential therapeutic strategies.
Descritores: Células-Tronco Neoplásicas/patologia
Diferenciação Celular/fisiologia
Resistencia a Medicamentos Antineoplásicos/fisiologia
Microambiente Tumoral/fisiologia
Carcinogênese/patologia
Autorrenovação Celular/fisiologia
-Prognóstico
Biomarcadores Tumorais/uso terapêutico
Camundongos SCID
Células Estromais/patologia
Matriz Extracelular/patologia
Microvasos/fisiopatologia
Evolução Clonal/fisiologia
Citometria de Fluxo
Corantes Fluorescentes
Limites: Animais
Camundongos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


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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-1179694
Autor: Abdallah, Emne Ali.
Título: Identificação de células tumorais circulantes e outros componentes sanguíneos em pacientes com câncer de cólon localizado / Identification of circulating tumor cells and other blood componentes in localized colon cancer.
Fonte: São Paulo; s.n; 2019. 148 p. ilust, tabelas, quadros.
Idioma: pt.
Tese: Apresentada a Fundação Antônio Prudente para obtenção do grau de Doutor.
Resumo: Introdução: A detecção precoce do câncer de cólon proporciona altas taxas de cura, no entanto, há pacientes que apresentam recidiva local e metástase à distância. As células tumorais circulantes (CTCs) e os microêmbolos circulantes (MEs) desempenham um papel importante nestes processos. Objetivo: avaliar o papel de CTCs e MEs em pacientes com câncer de cólon localizado. Material e métodos: foram coletados 10 mL de sangue de pacientes com câncer de cólon pré-cirúrgico, pré-adjuvância e 6 meses após o final do tratamento. As amostras foram processadas no dispositivo ISET® e as CTCs foram fixadas com formaldeído e identificadas por imunocitoquímica. Para detecção de expressão de RNAm, foi realizada a técnica de hibridização in situ cromogênica. O DNA foi extraído das membranas sem formaldeído e analisado por PCR digital em gotas. Resultados: no módulo I, foram incluídos 69 pacientes (18 com estágio I, 15 com estágio II e 36 com estágio III). A taxa de detecção de CTCs na primeira coleta foi de 94,2%, de 94,6% no primeiro seguimento e de 100% no segundo seguimento. Foi observada uma queda global na mediana de CTCs ao longo do tempo. No segundo seguimento, a expressão de ERCC1 e de ß-galactosidase nas CTCs foi mais encontrada em pacientes com estágio III (p= 0,03 e p= 0,04, respectivamente). A expressão de ERCC1 com alto índice de positividade (IP) nas CTCs, no segundo seguimento foi determinante de sobrevida livre de recidiva (SLR) inferior (p= 0,014). Foi encontrada uma correlação positiva entre o nível de CTCs e a porcentagem de células TReg (p= 0,01) e negativa entre o nível de CTCs e a porcentagem de linfócitos CD3+ (p= 0,01). Pacientes com alta Platelet-to-Lymphocyte Ratio (PLR) encontravam-se em sua maioria com estadiamentos patológicos II de alto risco e III (p= 0,014). Alta PLR foi determinante de SLR inferior (p= 0,01). No módulo II (pacientes com tumores de alto risco, submetidos à quimioterapia adjuvante) foi encontrada uma correlação positiva entre os níveis de CTC e CEA nos casos que tiveram recidiva da doença (p= 0,001). Alto IP de ERCC1 no segundo seguimento foi determinante de SLR significantemente inferior (p= 0,013). Conclusões: CTCs foram encontradas em altas taxas nos pacientes com câncer de cólon localmente avançado. A avaliação do sistema imunológico dos pacientes juntamente com as CTCs demonstrou ser uma ferramenta promissora para acompanhamento destes pacientes

Introduction: The early detection of colon cancer provides high cure rates, however, there are patients that present local relapse and distant metastasis. Circulating tumor cells (CTCs) and circulating tumor microemboli (CTM) play a crucial role in these processes. Objectives: to evaluate the role of CTCs and CTM in non-metastatic colon cancer patients. Material and methods: 10 mL of blood were collected from colon cancer patients prior to the surgery, prior to the adjuvant treatment, and 6 months after the treatment end. Samples were processed in the ISET® device and CTCs were formaldehyde-fixed and identified by immunocytochemistry. For mRNA expression in situ hybridization was applied. The DNA was extracted from the non-fixed CTCs and analyzed by droplet digital PCR. Results: there were 69 patients included (18 at stage I, 15 at stage II, and 36 at stage III) at module I. The CTC detection rate at baseline was 94.2%, at first follow-up was 94.6%, and at second follow-up was 100%. It was observed an overall drop in CTC median over time. At second follow-up, ERCC1 and ß-galactosidase expression in CTCs was most commonly found in stage III patients (p= 0.03 and p= 0.04, respectively). High positivity index (PI) of ERCC1 in CTC at second follow-up was determinant of inferior relapse-free survival (RFS) (p= 0.014). It was found a positive correlation between CTC levels and the percentage of TReg cells (p= 0.01) and a negative correlation between CTC levels and the percentage of CD3+ lymphocytes. Patients with high Platelet-to-Lymphocyte Ratio (PLR) were mostly found in high-risk stage II and III patients (p= 0.014). High PLR was determinant of inferior RFS (p= 0.01). At module II (patients with high-risk tumors, treated with adjuvant chemotherapy), it was found a positive correlation between CTC and CEA levels in the cases that shown disease progression (DP) (p= 0.001). High PI of ERCC1 at second follow-up had shown significantly worse RFS (p= 0.013). Conclusions: CTCs were found in high rates in localized colon cancer patients. Additionally, the evaluation of the patient's immune combined with the CTCs showed to be a promising tool to monitoring these patients
Descritores: Biomarcadores
Neoplasias Colorretais/cirurgia
Neoplasias Colorretais/terapia
Resistencia a Medicamentos Antineoplásicos
Células Neoplásicas Circulantes
-Neoplasias Colorretais/sangue
Biópsia Líquida
Limites: Humanos
Masculino
Feminino
Adulto
Pessoa de Meia-Idade
Idoso
Responsável: BR30.1 - Biblioteca
BR30.1


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Id: biblio-1181093
Autor: Perú. Ministerio de Salud. Dirección General de Medicamentos, Insumos y Drogas.
Título: Situación de los productos oncológicos de mayor impacto económico en el sistema de salud: Anticuerpos monoclonales / Situation of oncology products of greater economic impact on the health system: Monoclonal Antibodies.
Fonte: Lima; Perú. Ministerio de Salud. Dirección General de Medicamentos, Insumos y Drogas; Jun. 2015. 39 p. ilus.
Idioma: es.
Resumo: La presente publicación desarrolla acciones conducentes a mejorar la disponibilidad y accesibilidad al tratamiento oncológicos y reconoce la necesidad de abordar de forma prioritaria el acceso a los medicamentos biotecnológicos esenciales de alto costo en el sistema de salud, y de establecer mecanismos que permitan obtener los mismos a precios más asequibles, enmarcados dentro de la normatividad nacional, regional e internacional. En la primera sección se detalla los datos epidemiológicos de la enfermedad, de la evolución del presupuesto público asignado a los productos farmacéuticos para la prevención y control del cáncer, del consumo de los medicamentos oncológicos, y en especial de los biotecnológicos de mayor impacto económico, así como de adquisiciones del sector público. En la segunda sección, el análisis de los precios en la cadena de comercialización de los productos oncológicos biotecnológicos de la categoría anticuerpos monoclonales, seleccionado por su impacto económico en el sistema de salud público y su alto costo. y por último, la información acerca de las ventas mundiales, disponibilidad de ingredientes farmacéuticos activos y de productos farmacéuticos terminados de los productos oncológicos biotecnológicos de la categoría anticuerpos monoclonales, seleccionado por su impacto económico en el sistema de salud público y su alto costo
Descritores: Análise de Situação
Avaliação de Medicamentos
Diagnóstico da Situação de Saúde
Resistencia a Medicamentos Antineoplásicos
Serviço Hospitalar de Oncologia
-Peru
Tipo de Publ: Relatos de Casos
Responsável: PE18.1 - Biblioteca Central
[{"text": "PE18.1", "_a": "MS/DIGEMID 0080", "_b": "(Formato Digital)"}]


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Id: biblio-1151503
Autor: Perú. Ministerio de Salud. Dirección General de Medicamentos, Insumos y Drogas.
Título: Situación de los productos oncológicos de mayor impacto económico en el sistema de salud: Anticuerpos monoclonales / Situation of oncology products of greater economic impact on the health system: Monoclonal Antibodies.
Fonte: Lima; Perú. Ministerio de Salud. Dirección General de Medicamentos, Insumos y Drogas; Jun. 2015. 38 p. ilus.
Idioma: es.
Resumo: Desarrolla acciones conducentes a mejorar la disponibilidad y accesibilidad al tratamiento oncológicos y reconoce la necesidad de abordar de forma prioritaria el acceso a los medicamentos biotecnológicos esenciales de alto costo en el sistema de salud, y de establecer mecanismos que permitan obtener los mismos a precios más asequibles, enmarcados dentro de la normatividad nacional, regional e internacional. En la primera sección se detalla los datos epidemiológicos de la enfermedad, de la evolución del presupuesto público asignado a los productos farmacéuticos para la prevención y control del cáncer, del consumo de los medicamentos oncológicos, y en especial de los biotecnológicos de mayor impacto económico, así como de adquisiciones del sector público. En la segunda sección, el análisis de los precios en la cadena de comercialización de los productos oncológicos biotecnológicos de la categoría anticuerpos monoclonales, seleccionado por su impacto económico en el sistema de salud público y su alto costo. y por último, la información acerca de las ventas mundiales, disponibilidad de ingredientes farmacéuticos activos y de productos farmacéuticos terminados de los productos oncológicos biotecnológicos de la categoría anticuerpos monoclonales, seleccionado por su impacto económico en el sistema de salud público y su alto costo
Descritores: Diagnóstico da Situação de Saúde
Serviço Hospitalar de Oncologia
Resistencia a Medicamentos Antineoplásicos
Análise de Situação
Avaliação de Medicamentos
Tipo de Publ: Relatos de Casos
Responsável: PE18.1 - Biblioteca Central


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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


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Id: biblio-1011415
Autor: Viscarra, Tamara; Buchegger, Kurt; Jofre, Ignacio; Riquelme, Ismael; Zanella, Louise; Abanto, Michel; Parker, Alyssa C; Piccolo, Stephen R; Roa, Juan Carlos; Ili, Carmen; Brebi, Priscilla.
Título: Functional and transcriptomic characterization of carboplatin-resistant A2780 ovarian cancer cell line
Fonte: Biol. Res;52:13, 2019. graf.
Idioma: en.
Projeto: National Commission for Scientific and Technological Research (CONICYT); . National Funding for Scientific and Technologic Development of Chile (FONDECYT); . Dirección de Investigación, Universidad de La Frontera (DIUFRO).
Resumo: BACKGROUND: Ovarian cancer is a significant cancer-related cause of death in women worldwide. The most used chemotherapeutic regimen is based on carboplatin (CBDCA). However, CBDCA resistance is the main obstacle to a better prognosis. An in vitro drug-resistant cell model would help in the understanding of molecular mechanisms underlying this drug-resistance phenomenon. The aim of this study was to characterize cellular and molecular changes of induced CBDCA-resistant ovarian cancer cell line A2780. METHODS: The cell selection strategy used in this study was a dose-per-pulse method using a concentration of 100 µM for 2 h. Once 20 cycles of exposure to the drug were completed, the cell cultures showed a resistant phenotype. Then, the ovarian cancer cell line A2780 was grown with 100 µM of CBDCA (CBDCA-resistant cells) or without CBDCA (parental cells). After, a drug sensitivity assay, morphological analyses, cell death assays and a RNA-seq analysis were performed in CBDCA-resistant A2780 cells. RESULTS: Microscopy on both parental and CBDCA-resistant A2780 cells showed similar characteristics in morphology and F-actin distribution within cells. In cell-death assays, parental A2780 cells showed a significant increase in phosphatidylserine translocation and caspase-3/7 cleavage compared to CBDCA-resistant A2780 cells (P < 0.05 and P < 0.005, respectively). Cell viability in parental A2780 cells was significantly decreased compared to CBDCA-resistant A2780 cells (P < 0.0005). The RNA-seq analysis showed 156 differentially expressed genes (DEGs) associated mainly to molecular functions. CONCLUSION: CBDCA-resistant A2780 ovarian cancer cells is a reliable model of CBDCA resistance that shows several DEGs involved in molecular functions such as transmembrane activity, protein binding to cell surface receptor and catalytic activity. Also, we found that the Wnt/3-catenin and integrin signaling pathway are the main metabolic pathway dysregulated in CBDCA-resistant A2780 cells.
Descritores: Neoplasias Ovarianas/genética
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Carboplatina/farmacologia
Resistencia a Medicamentos Antineoplásicos/genética
Transcriptoma/efeitos dos fármacos
Antineoplásicos/farmacologia
-Neoplasias Ovarianas/patologia
Neoplasias Ovarianas/tratamento farmacológico
Fenótipo
Transdução de Sinais
Morte Celular/efeitos dos fármacos
Morte Celular/genética
Análise de Sequência de RNA
Linhagem Celular Tumoral
Transcriptoma/genética
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central



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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde