Base de dados : LILACS
Pesquisa : G04.712 [Categoria DeCS]
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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


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Id: biblio-1011400
Autor: Sun, Deyu; Mu, Yi; Piao, Haozhe.
Título: MicroRNA-153-3p enhances cell radiosensitivity by targeting BCL2 in human glioma
Fonte: Biol. Res;51:56, 2018. graf.
Idioma: en.
Resumo: BACKGROUND: Glioma is the most prevalent malignant tumor in human central nervous systems. Recently, the development of resistance to radiotherapy in glioma patients markedly vitiates the therapy outcome. MiR-153-3p has been reported to be closely correlated with tumor progression, but its effect and molecular mechanism underlying radioresistance remains unclear in glioma. METHODS: The expression of miR-153-3p was determined in radioresistant glioma clinical specimens as well as glioma cell lines exposed to irradiation (IR) using quantitative real-time PCR. Cell viability, proliferation and apoptosis were then evaluated by MTT assay, colony formation assay, Flow cytometry analysis and caspase-3 activity assay in glioma cells (U87 and U251). Tumor forming was evaluated by nude mice model in vivo. TUNEL staining was used to detect cell apoptosis in nude mice model. The target genes of miR-153-3p were predicted and validated using integrated bioinformatics analysis and a luciferase reporter assay. RESULTS: Here, we found that miR-153-3p was down-regulated in radioresistant glioma clinical specimens as well as glioma cell lines (U87 and U251) exposed to IR. Enhanced expression of miR-153-3p promoted the radiosensitivity, promoted apoptosis and elevated caspase-3 activity in glioma cells in vitro, as well as the radiosensitivity in U251 cell mouse xenografs in vivo. Mechanically, B cell lymphoma-2 gene (BCL2) was identified as the direct and functional target of miR-153-3p. Moreover, restoration of BCL2 expression reversed miR-153-3p-induced increase of radiosensitivity, apoptosis and caspase-3 activity in U251 cells in vitro. In addition, clinical data indicated that the expression of miR-153-3p was significantly negatively associated with BCL2 in radioresistance of glioma samples. CONCLUSIONS: Our findings suggest that miR-153-3p is a potential target to enhance the effect of radiosensitivity on glioma cells, thus representing a new potential therapeutic target for glioma.
Descritores: Tolerância a Radiação/genética
Genes bcl-2/fisiologia
MicroRNAs/efeitos da radiação
MicroRNAs/fisiologia
Glioma/genética
-Fatores de Tempo
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
Sobrevivência Celular/efeitos da radiação
Western Blotting
Análise de Variância
Marcação de Genes/métodos
Genes bcl-2/efeitos da radiação
Marcação In Situ das Extremidades Cortadas
MicroRNAs/análise
Linhagem Celular Tumoral
Proliferação de Células/efeitos da radiação
Caspase 3/análise
Reação em Cadeia da Polimerase em Tempo Real
Citometria de Fluxo
Glioma/radioterapia
Limites: Humanos
Masculino
Feminino
Adulto
Pessoa de Meia-Idade
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-973869
Autor: Bravo-Filho, Vasco; Logan, Patrick; Zoroquiain, Pablo; Aldrees, Sultan; Vilà, Natàlia; Oweida, Ayman; Belfort Neto, Rubens; Burnier Jr, Miguel N.
Título: Effects of ranibizumab and amfenac on the functional abilities and radiosensitivity of uveal melanoma cells / Efeitos do ranibizumabe e do amfenac nas habilidades funcionais e na radiossensibilidade de células de melanoma uveal
Fonte: Arq. bras. oftalmol;82(1):38-44, Jan.-Feb. 2019. tab, graf.
Idioma: en.
Resumo: ABSTRACT Purpose: To evaluate the effects of ranibizumab and amfenac in human uveal melanoma cell lines and to explore the ability of these compounds to sensitize uveal melanoma cells to radiation therapy. Methods: The 92.1 human uveal melanoma cell line was cultured and subjected to the proposed treatment (ranibizumab, amfenac, and a combination of both). Proliferation, migration, and invasion assays of the 92.1 uveal melanoma cell line were assessed after pretreatment with ranibizumab (125 mg/mL), amfenac (150 nM), or a combination of both. In addition, proliferation rates were assessed after treatment with ranibizumab and amfenac, and the cells were subsequently exposed to various radiation doses (0, 4, and 8 Gy). Results: Proliferation assay: cells treated with a combination of ranibizumab and amfenac had lower proliferation rates than controls (p=0.016) and than those treated with only ranibizumab (p=0.033). Migration assay: a significantly lower migration rate was observed in cells treated with amfenac than the control (p=0.014) and than those treated with ranibizumab (p=0.044). Invasion assay: there were no significant differences among the studied groups. Irradiation exposure: in the 4 Gy dose group, there were no significant differences among any groups. In the 8 Gy dose group, treatment with ranibizumab, amfenac, and their combination prior to application of the 8 Gy radiation led to a marked reduction in proliferation rates (p=0.009, p=0.01, and p=0.034, respectively) compared with controls. Conclusion: Combination of ranibizumab and amfenac reduced the proliferation rate of uveal melanoma cells; however, only amfenac monotherapy significantly decreased cell migration. The radiosensitivity of the 92.1 uveal melanoma cell line increased following the administration of ranibizumab, amfenac, and their combination. Further investigation is warranted to determine if this is a viable pretreatment strategy to render large tumors amenable to radiotherapy.

RESUMO Objetivo: Avaliar os efeitos do ranibizumabe em associação com o amfenac nas células de melanoma uveal humano e explorar a capacidade desses compostos em sensibilizar as células de melanoma uveal à radioterapia. Métodos: Células de melanoma uveal humano do tipo 92.1 foram cultivadas e submetidas ao tratamento proposto (ranibizumabe, amfenac e a combinação de ambos). Ensaios de proliferação, migração e invasão com as células de melanoma uveal do tipo 92.1 foram avaliados após tratamento com ranibizumabe (125 mg/ml), amfenac (150 nM) e a combinação de ambos. Além disso, as taxas de proliferação foram avaliadas após tratamento com ranibizumabe e amfenac com subsequente exposição das células a diferentes doses de radiação (0 Gy, 4 Gy e 8 Gy). Resultados: Ensaio de proliferação: células tratadas com ranibizumabe e amfenac combinados apresentaram taxas de proliferação inferiores em comparação ao grupo controle (p=0,016), do que as tratadas apenas com ranibizumabe (p=0,033). Ensaio de migração: foi observada uma taxa de migração significativamente mais baixa nas células tratadas com amfenac do que no grupo controle (p=0,014) e do que nas tratadas com ranibizumabe (p=0,044). Ensaio de invasão: não houve diferenças significativas entre os grupos estudados. Exposição à irradiação: no grupo da dose de 4 Gy, não houve diferença significante entre os grupos. No grupo da dose de 8 Gy, o tratamento com ranibizumabe, afenac e sua combinação antes da aplicação da radiação de 8 Gy levou a uma redução acentuada nas taxas de proliferação (p=0,009, p=0,01 e p=0,034, respectivamente) em comparação aos grupos controle. Conclusão: A combinação de ranibizumabe e amfenac reduziu a taxa de proliferação das células de melanoma uveal; no entanto, apenas o amfenac diminuiu significativamente a migração celular. A radiossensibilidade das células de melanoma uveal do tipo 92.1 aumentou após a administração de ranibizumabe, amfenac e sua combinação. Mais investigações são necessárias para determinar se esta é uma estratégia de pré-tratamento viável para tornar grandes tumores passíveis de radioterapia.
Descritores: Fenilacetatos/farmacologia
Inibidores da Angiogênese/farmacologia
Inibidores de Ciclo-Oxigenase 2/farmacologia
Ranibizumab/farmacologia
Melanoma/tratamento farmacológico
Melanoma/radioterapia
-Tolerância a Radiação
Neoplasias Uveais/tratamento farmacológico
Neoplasias Uveais/radioterapia
Protocolos de Quimioterapia Combinada Antineoplásica
Movimento Celular/efeitos dos fármacos
Movimento Celular/efeitos da radiação
Reprodutibilidade dos Testes
Linhagem Celular Tumoral
Proliferação de Células/efeitos dos fármacos
Proliferação de Células/efeitos da radiação
Relação Dose-Resposta à Radiação
Limites: Humanos
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


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Id: biblio-838415
Autor: Schmidt, Angelica; Iglesias, Laura; Klain, Michele; Pitoia, Fabián; Schlumberger, Martin J.
Título: Radioactive iodine-refractory differentiated thyroid cancer: an uncommon but challenging situation
Fonte: Arch. endocrinol. metab. (Online);61(1):81-89, Jan.-Feb. 2017. tab.
Idioma: en.
Resumo: ABSTRACT Radioiodine (RAI)-refractory thyroid cancer is an uncommon entity, occurring with an estimated incidence of 4-5 cases/year/million people. RAI refractoriness is more frequent in older patients, in those with large metastases, in poorly differentiated thyroid cancer, and in those tumors with high 18-fluordeoxyglucose uptake on PET/CT. These patients have a 10-year survival rate of less than 10%. In recent years, new therapeutic agents with molecular targets have become available, with multikinase inhibitors (MKIs) being the most investigated drugs. Two of these compounds, sorafenib and lenvatinib, have shown significant objective response rates and have significantly improved the progression-free survival in the two largest published prospective trials on MKI use. However, no overall survival benefit has been achieved yet. This is probably related to the crossover that occurs in most patients who progress on placebo treatment to the open treatment of these studies. In consequence, the challenge is to correctly identify which patients will benefit from these treatments. It is also crucial to understand the appropriate timing to initiate MKI treatment and when to stop it. The purpose of this article is to define RAI refractoriness, to summarize which therapies are available for this condition, and to review how to select patients who are suitable for them.
Descritores: Neoplasias da Glândula Tireoide/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
Radioisótopos do Iodo/uso terapêutico
Antineoplásicos/uso terapêutico
-Tolerância a Radiação
Neoplasias da Glândula Tireoide/mortalidade
Neoplasias da Glândula Tireoide/radioterapia
Falha de Tratamento
Retratamento
Gerenciamento Clínico
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Amaral, Ademir
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Id: biblio-886652
Autor: SANTOS, NEYLIANE F G DOS; SILVA, RAFAEL F; PINTO, MARCELA M P L; SILVA, EDVANE B DA; TASAT, DEBORAH R; AMARAL, ADEMIR.
Título: Active caspase-3 expression levels as bioindicator of individual radiosensitivity
Fonte: An. acad. bras. ciênc;89(1,supl):649-659, May. 2017. graf.
Idioma: en.
Resumo: ABSTRACT Several molecules and events involved in cell response to radiation-induced damage have been investigated towards a personalized radiotherapy. Considering the importance of active caspase-3 in the proteolytic cascade that ensures radiation-induced apoptosis execution, this research was designed to evaluate the expression levels of this protein as a bioindicator of individual radiosensitivity. Peripheral blood samples of 10 healthy individuals were gamma-irradiated (cobalt-60 source) with 1, 2 and 4 Gy (control: non-irradiated samples), and active caspase-3 expression levels were measured in lymphocytes, by flow cytometry, ex vivo and after different times of in vitro incubation (24, 48 and 72 hours). Short-term incubation of 24 h was the most adequate condition to evidence correlations between dose radiation and active caspase-3 expression. For each radiation dose, it was observed a significant inter-individual variation in active caspase-3 expression intensity, suggesting that this parameter may be suitable for evidence individual radiosensitivity. The methodology presented and discussed in this work may help to predict healthy tissues response to radiation exposure toward the better patient outcome.
Descritores: Tolerância a Radiação/efeitos da radiação
Linfócitos/efeitos da radiação
Radioisótopos de Cobalto
Apoptose/efeitos da radiação
Caspase 3/metabolismo
-Linfócitos/enzimologia
Biomarcadores Ambientais
Relação Dose-Resposta à Radiação
Citometria de Fluxo
Limites: Humanos
Masculino
Feminino
Adulto
Responsável: BR1.1 - BIREME


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Id: lil-673030
Autor: Ramos, Adriano de Paula; Marques, Gustavo Inácio de Gomes; Mendonça, Yuri de Abreu; Dourado, Juliana Castro; Soares, Renata de Bastos Ascenço.
Título: Clinical evaluation of normal tissue toxicity induced by ionizing radiation in cases of larygeal carcinoma
Fonte: Appl. cancer res;32(3):60-63, 2012. tab.
Idioma: en.
Resumo: Laryngeal cancer is the second most frequent head and neck cancer in the Brazilian male population. For treatment, radiotherapy combined with chemotherapy is now used in substitution for total laryngectomy, becoming the standard treatment for advanced larynx cancer cases, with the aim of organ preservation. However, this method needs assessment of the side effects caused to normal tissue and organ functionality after treatment and the relation of these clinical factors to the individual characteristics of patients. Thus, the clinical characteristics of 229 patients with laryngeal cancer treated with radiotherapy were evaluated by medical records analysis in relation to normal tissue radiosensibility. Significant relations between smoking (p = 0.018) and combined chemoradiotherapy assistance (p = 0.03) were identified with high frequency of treatment suspension cases. The application of combined chemoradiotherapy also resulted in a higher incidence of oral mucositis (p = 0.04), xerostomia (p = 0.001) and treatment side effects to GIT (p = 0.04). Advanced clinical staging was associated with worse prognosis (p = 0.002) and a higher occurrence of treatment failure (p < 0.001). Radiotherapy was also less effective depending on the primary tumor location (p = 0.001)
Descritores: Neoplasias Laríngeas/terapia
Radioterapia/efeitos adversos
Tolerância a Radiação
Toxicidade/efeitos adversos
Limites: Humanos
Masculino
Tipo de Publ: Ensaio Clínico
Responsável: BR30.1 - Biblioteca


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Id: lil-233814
Autor: Khoury, Helen; Amaral, Ademir; Hazin, Clovis; Melo, Francisco.
Título: Estudo da resposta de fotodiodos para dosimetria beta / Study of response of photodiode to beta dosimetry
Fonte: In: Schiabel, Homero; Slaets, Annie France Frère; Costa, Luciano da Fontoura; Baffa Filho, Oswaldo; Marques, Paulo Mazzoncini de Azevedo. Anais do III Fórum Nacional de Ciência e Tecnologia em Saúde. Säo Carlos, s.n, 1996. p.452-452, tab, graf.
Idioma: pt.
Conferência: Apresentado em: Fórum Nacional de Ciência e Tecnologia em Saúde, 3 e Congresso Brasileiro de Engenharia Biomédica, 15 e Congresso Brasileiro de Físicos em Medicina , 6 e Congresso Brasileiro de Informática em Saúde, 5 e Encontro Brasileiro de Proteçäo Radiológica, Campos do Jordäo, 13-17 out. 1996.
Resumo: Neste trabalho foram analisadas as respostas dos fotodiodos comerciais SFH-206, BPY-12 e BPW-34 para uso em dosimetria beta. O resultado obtidos mostram que as respostas destes fotodiodos variam linearmente com a dose, apresentando um desvio menor que 1 por cento. O fotodiodo BPY-12 demonstrou ser mais sensível à radiação do que os outros dois fotodiodos estudados.
Descritores: Dosimetria/instrumentação
Tolerância a Radiação
-Dosimetria Termoluminescente/estatística & dados numéricos
Tratamento Térmico
Responsável: BR1.1 - BIREME
BR1.1/3012.06


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Id: biblio-889093
Autor: Chen, Changxuan; Wang, Kaizhen; Wang, Qian; Wang, Xin.
Título: LncRNA HULC mediates radioresistance via autophagy in prostate cancer cells
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;51(6):e7080, 2018. graf.
Idioma: en.
Resumo: Prostate cancer (PCa) is the second leading cause of cancer death in men. Irradiation is one of the available options for treatment of PCa, however, approximately 10-45% of PCa are resistant to irradiation. We aimed to explore the role of long non-coding RNA highly upregulated in liver cancer (HULC) in the sensitivity of PCa cells to irradiation. Survival rate, cell apoptosis, cycle, expressions of related proteins, and caspase-3 activity were assessed to explore the effects of HULC on sensitivity of PCa cells to irradiation. Expression of HULC in DU-145, PC3, LNCaP, and RWPE-1 cells was determined and the influence of HULC on DU-145 cells was explored. Then, PC3 cells aberrantly expressing HULC were implanted into NOD-SCID mice for tumor xenograft study. Changes of autophagy after aberrant expression of HULC in vivo and in vitro were tested. Furthermore, the interacted protein of HULC and involved signaling pathway were investigated. In PC3 and LNCaP cells under irradiation, survival rate and cell cycle were decreased and apoptosis was increased by HULC knockdown. HULC knockdown arrested PC3 cells at G0/G1 phase. DU-145 was sensitive to irradiation, and resistance to irradiation of DU-145 cells was enhanced by HULC overexpression. Moreover, HULC knockdown enhanced the sensitivity of PC3 xenografts to irradiation. HULC knockdown promoted autophagy through interaction with Beclin-1 and inhibition of mTOR, resulting in increased apoptosis. HULC knockdown improved sensitivity of PCa cells to irradiation both in vivo and in vitro. HULC suppressed Beclin-1 phosphorylation, thereby reduced autophagy, involving the mTOR pathway.
Descritores: Autofagia/efeitos da radiação
Neoplasias da Próstata/patologia
Tolerância a Radiação/fisiologia
RNA Longo não Codificante/efeitos da radiação
-Apoptose/efeitos da radiação
Western Blotting
Linhagem Celular Tumoral/efeitos da radiação
Reação em Cadeia da Polimerase em Tempo Real
Interferência de RNA/efeitos da radiação
Transfecção
Limites: Humanos
Masculino
Responsável: BR1.1 - BIREME


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Id: lil-757384
Autor: Joaquim, Andrei F.; Powers, Ann; Laufer, Ilya; Bilsky, Mark H..
Título: An update in the management of spinal metastases / Atualização no manejo das metástases na coluna vertebral
Fonte: Arq. neuropsiquiatr;73(9):795-802, Sept. 2015. tab, ilus.
Idioma: en.
Resumo: The best clinical treatment for spinal metastases requires an integrated approach with input from an interdisciplinary cancer team. The principle goals of treatment are maintenance or improvement in neurologic function and ambulation, spinal stability, durable tumor control, and pain relief. The past decade has witnessed an explosion of new technologies that have impacted our ability to reach these goals, such as separation surgery and minimally invasive spinal procedures. The biggest advance, however, has been the evolution of stereotactic radiosurgery that has demonstrated durable tumor control both when delivered as definitive therapy and as a postoperative adjuvant even for tumors considered markedly resistant to conventional external beam radiation. In this paper, we perform an update on the management of spinal metastases demonstrating the integration of these new technologies into a decision framework NOMS that assesses four basic aspects of a patient’s spine disease: Neurologic, Oncologic, Mechanical Instability and Systemic disease.

O tratamento dos pacientes com metástases na coluna requer uma abordagem multidisciplinar por equipe especializada em oncologia. Os objetivos básicos do tratamento são a manutenção/ melhora da função neurológica com preservação da deambulação, manutenção da estabilidade da coluna, controle tumoral e alívio da dor. A última década testemunhou uma explosão de novas tecnologias que auxiliaram a atingir os objetivos terapêuticos, como a cirurgia de separação e procedimentos minimamente cirúrgicos minimamente invasivos. Contudo, o maior avanço terapêutico constitui-se do uso da radiocirurgia no tratamento das metástases de coluna, que possibilita bom controle local tanto como terapia definitiva ou no pós-operatório de tumores, mesmo os considerados radioresistentes à radioterapia convencional. No presente artigo, realizamos atualização do manejo das metástases de coluna, apresentando a integração das novas tecnologias em um algoritmo de decisão “NOMS” que inclui os quatros aspectos básicos dos pacientes com metástases na coluna:Neurologic, Oncologic, Mechanical InstabilityeSystemic disease.
Descritores: Neoplasias da Coluna Vertebral/secundário
Neoplasias da Coluna Vertebral/terapia
-Terapia Combinada
Tomada de Decisões
Tolerância a Radiação
Radiocirurgia
Compressão da Medula Espinal/terapia
Doenças da Coluna Vertebral/diagnóstico
Doenças da Coluna Vertebral/cirurgia
Neoplasias da Coluna Vertebral/diagnóstico
Resultado do Tratamento
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: lil-753968
Autor: Zou, Kun; Liu, Caigang; Zhang, Zhuo; Zou, Lijuan.
Título: The effect of elemene on lung adenocarcinoma A549 cell radiosensitivity and elucidation of its mechanism
Fonte: Clinics;70(8):556-562, 08/2015. tab, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China.
Resumo: OBJECTIVE: To investigate the effect of elemene on the radiosensitivity of A549 cells and its possible molecular mechanism. METHODS: Apoptosis of A549 cells was detected by flow cytometry and fluorescence microscopy. The effect of double-strand break (DSB) damage repair in A549 cells was evaluated using the neutral comet assay. Protein expression levels were detected using western blotting, and the correlation between protein levels was analyzed. RESULTS: Elemene exhibited a radiosensitizing effect on A549 cells. The level of apoptosis induced by elemene combined with radiation was significantly greater (p<0.01) than that elicited by either radiation or elemene alone. Following radiation and subsequent repair for 24 h, the tail intensity of A549 cells treated with a combination of elemene and radiation was greater than that of cells treated with either elemene or radiation alone (p<0.01). This result indicates that elemene inhibits cellular DSB repair. Both elemene combined with radiation and radiation alone decreased the protein expression of DNA-PKcs and Bcl-2 compared to elemene alone (p<0.01), while p53 protein expression was increased (p<0.01). A negative correlation was observed between DNA-PKcs and p53 expression (r=−0.569, p=0.040), while a positive correlation was found between DNA-PKcs and Bcl-2 expression (r=0.755, p=0.012). CONCLUSIONS: Elemene exhibits a radiosensitizing effect on A549 cells, and its underlying molecular mechanism of action may be related to the downregulation of DNA-PKcs gene expression. .
Descritores: Adenocarcinoma/radioterapia
Neoplasias Pulmonares/radioterapia
Tolerância a Radiação/efeitos da radiação
Radiossensibilizantes/farmacologia
Sesquiterpenos/farmacologia
-Análise de Variância
Adenocarcinoma/tratamento farmacológico
Adenocarcinoma/genética
Apoptose/efeitos dos fármacos
Apoptose/efeitos da radiação
Western Blotting
Linhagem Celular Tumoral
Ensaio Cometa
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos da radiação
Reparo do DNA/efeitos dos fármacos
Reparo do DNA/efeitos da radiação
Proteína Quinase Ativada por DNA/metabolismo
Citometria de Fluxo
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos da radiação
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/genética
Microscopia de Fluorescência
Doses de Radiação
Tolerância a Radiação/efeitos dos fármacos
/metabolismo
TUMOR SUPPRESSOR PROTEIN PDIPETALONEMA INFECTIONS/metabolismo
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME



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