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Id: biblio-973381
Autor: Oliveira, Levindo Alves de; Oshima, Celina Tizuko Fujiyama; Soffner, Pedro Augusto; Silva, Marcelo de Souza; Lins, Rodrigo Rego; Malinverni, Andréa Cristina de Moraes; Waisberg, Jaques.
Título: The canonical wnt pathway in gastric carcinoma / Via canônica do wnt no carcinoma gástrico
Fonte: ABCD arq. bras. cir. dig;32(1):e1414, 2019. tab, graf.
Idioma: en.
Resumo: ABSTRACT Background : It is believed that the Wnt pathway is one of the most important signaling involved in gastric carcinogenesis. Aim : To analyze the protein expression of canonical and non-canonical Wnt pathways in gastric carcinoma. Method : The immunohistochemistry was performed in 72 specimens of gastric carcinomas for evaluating the expression of Wnt-5a, FZD5, GSK3β, axin, CK1, ubiquitin, cyclin D1 and c-myc. Results : There were significant differences for cytoplasm and nucleus ubiquitin for moderately and well differentiated tumors (p=0.03) and for those of the intestinal type of the Lauren classification (p=0.03). The absence of c-myc was related to Lauren's intestinal tumors (p=0.03). Expression of CK1 in the cytoplasm was related to compromised margin (p=0.03). Expression of cyclin D1 protein was more intense in male patients (p=0.03) There was no relation of the positive or negative expression of the Wnt-5a, FZD5, GSK3 and Axin with any clinicopathological variables. Conclusion: The canonical WNT pathway is involved in gastric carcinoma.

RESUMO Racional : Acredita-se que a via Wnt é uma das mais importantes da sinalização envolvidas na carcinogênese gástrica. Objetivos : Analisar a expressão das proteínas das vias Wnt canônicas e não-canônicas no carcinoma gástrico e relacionar sua expressão com as variáveisclinicopatológicas. Método : Foram coletadas 72 amostras de carcinoma gástrico, e áreas representativas do tumor foram selecionadas para o Tissue Microarray. Imunoistoquímica foi realizada para avaliar a expressão de Wnt-5a, FZD5, GSK3β, axina, CK1, ubiquitina, ciclina D1 e c-myc. Resultados : Houve diferenças significativas para a expressão de ubiquitina no citoplasma e núcleo para tumores moderadamente e bem diferenciados (p=0,03) e para aqueles do tipo intestinal da classificação de Lauren (p=0,03). A expressão negativa da proteína c-myc no citoplasma foi relacionada aos tumores intestinais de Lauren (p=0,028). A expressão positiva de CK1 no citoplasma das células neoplásicas foi relacionada a tumores com margens cirúrgicas livre de envolvimento neoplásico (p=0,03). A expressão positiva da proteína ciclina D1 foi maior nos tumores dos homens (p=0,03). Não houve relação da expressão positiva ou negativa das proteínas Wnt-5a e FZD5 no citoplasma ou núcleo com quaisquer variáveis clinicopatológicas. O mesmo foi observado para GSK3β e Axin. Conclusões : A relação da expressão das proteínas da via canônica com as variáveis epidemiológicas e tumorais sugere sua participação na carcinogênese gástrica. Por outro lado, a ausência da relação das expressões das proteínas da via não-canônica sugere sua não participação na carcinogênese gástrica.
Descritores: Neoplasias Gástricas/química
Carcinoma/química
Via de Sinalização Wnt
Proteínas de Neoplasias/análise
-Valores de Referência
Neoplasias Gástricas/patologia
Imuno-Histoquímica
Carcinoma/patologia
Proteínas Proto-Oncogênicas c-myc/análise
Ciclina D1/análise
Ubiquitina/análise
Caseína Quinase I/análise
Receptores Frizzled/análise
Proteína Axina/análise
Carcinogênese
Glicogênio Sintase Quinase 3 beta/análise
Proteína Wnt-5a/análise
Estadiamento de Neoplasias
Limites: Humanos
Masculino
Feminino
Responsável: BR1.1 - BIREME


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Id: biblio-960035
Autor: Rosero G, Carol Yovanna; Corredor, Mauricio; Mejía O, Lizeth.
Título: Polimorfismos en genes implicados en el desarrollo de cáncer gástrico: revisión / A Review of Polymorphisms in Genes Involved in the Development of Gastric Cancer
Fonte: Rev. colomb. gastroenterol;31(4):391-402, oct.-dic. 2016. ilus, tab.
Idioma: es.
Resumo: El carcinoma o linfoma gástrico es una de las principales causas de mortalidad por cáncer en el mundo. Esta enfermedad es el resultado final de un largo proceso multifactorial en el que interviene un elevado número de factores ambientales y genéticos. Como enfermedad genética, la variación individual en riesgo de cáncer ha sido asociada con variantes alélicas específicas de diferentes genes (polimorfismos), en los cuales se hallan los mecanismos moduladores que dan respuesta a la carcinogénesis y el riesgo de progreso de la misma. De esta manera, las investigaciones a nivel molecular se han enfocado en la detección de las alteraciones en la conformación de bases sobre genes de predisposición al desarrollo y progresión del cáncer gástrico. Estos estudios fueron realizados en diversas poblaciones donde la enfermedad es recurrente, basados inicialmente en la selección individual de polimorfismo de nucleótido simple (SNP) en genes candidatos. Importantes marcadores moleculares han sido descritos y propuestos como marcadores pronóstico en este tipo de pacientes y permiten así el avance en el entendimiento del proceso neoplásico. Esta revisión pretende dar una mirada de actualización en los estudios recientes en polimorfismos de genes implicados en procesos inmunogenéticos, en mecanismos de reparación de ADN, en la respuesta a la desintoxicación de compuestos carcinógenos y en mecanismos de supresión tumoral o que intervienen en la apoptosis, procesos que están involucrados en el desarrollo de cáncer gástrico. Datos de marcadores moleculares asociados con esta enfermedad de genomas de colombianos y foráneos ya almacenados en las bases de datos del proyecto 1000 Genomes son también reportados

Gastric carcinoma and lymphoma are leading causes of cancer mortality throughout the world. This disease is the end result of a long multifactorial process involving a large number of environmental and genetic factors. As a genetic disease, individual variation in cancer risk has been associated with specific alleles of different genes (polymorphisms) in which the modulatory mechanisms of carcinogenesis and the risk of its progression are found. Research at the molecular level has focused on the detection of genetic alterations predisposing to the development and progression of gastric cancer. These studies have been conducted in various populations in which the disease recurs and have been initially based on individual selection of single nucleotide polymorphisms (SNPs) in candidate genes. Important molecular markers have been described and proposed as prognostic markers in this type of patients which has allowed for advances in the understanding of the neoplastic process. This review intends to provide an up to date look at recent studies on gene polymorphisms involved in immunogenic processes, DNA repair mechanisms, responses to detoxification of carcinogenic compounds, mechanisms of tumor suppression and apoptosis which are all processes involved in the development of gastric cancer. Data are also reported from molecular markers associated with this disease from Colombian and foreign genomes already stored in the database of the 1000 Genomes Project.
Descritores: Pesquisa
Neoplasias Gástricas
Polimorfismo de Nucleotídeo Único
Carcinogênese
Genética
Doenças Genéticas Inatas
-Genes
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CO354 - Sociedad Colombiana de Gastroenterología


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Id: biblio-990026
Autor: Carranza-Martínez, Brisa D; Salas-Treviño, Daniel; Soto-Domínguez, Adolfo; Ramírez-Romero, Rafael; Zapata-Benavides, Pablo; Cedillo-Rosales, Sibilina; Zárate-Ramos, Juan José; Saucedo-Cárdenas, Odila; Zamora-Ávila, Diana E.
Título: WT1 expression as a potential biomarker of malignancy in canine breast tumor / La expresión de WT1 como un biomarcador potencial maligno en un tumor de mama canino
Fonte: Int. j. morphol;37(1):190-195, 2019. graf.
Idioma: en.
Resumo: SUMMARY: Veterinary oncology is very important nowadays to get a better understanding of human carcinogenesis. Estrogen receptor, progesterone receptor and Human Epidermal Growth Factor receptor 2 are frequently evaluated by immunohistochemistry (HIC) in human breast tumor. WT1 is an oncogene, its overexpression has been detected in leukemia and diverse solid tumors like breast cancer, lung cancer and mesothelioma in humans. WT1 expression was evaluated in 15 canine breast tumors (CBT) diagnosed by histopathological analysis to find its relationship with neoplasia and malignancy. IHC and RT-PCR were performed in CBT tissues. Fisher´s test was used to analyze WT1 relationship with malignancy. Of the 15 tumors, 9 (60 %) were diagnosed as benign and 6 (40 %) were malignant. With IHC, WT1 expression was positive only in biopsies diagnosed as malignant. Expression of WT1 by RT-PCR was detected in 14 of the 15 tumors (93.33 %) as well as in control healthy mammary gland. Clinical significance: This study describes for the first time a close correlation between CBT and a positive result for WT1 expression with IHC; hence, it can be used as a biomarker for this neoplasia and as an indicator of malignancy. RT-PCR analysis also showed to be good option to detect WT1 expression. These results will be useful to further investigations to elucidate WT1-related signaling pathways in CBT. Also to know molecules that regulate the translation of this protein as a marker for tumor progression.

RESUMEN: La oncología veterinaria es muy importante hoy en día para comprender mejor la carcinogénesis humana. El receptor de estrógeno, el receptor de progesterona y el receptor 2 del factor de crecimiento epidérmico humano se evalúan con frecuencia mediante inmunohistoquímica (HIC) en tumores de mama humanos. WT1 es un oncogén, su sobreexpresión se ha detectado en leucemia y en diversos tumores sólidos como el cáncer de mama, cáncer de pulmón y mesotelioma en humanos. La expresión de WT1 se evaluó en 15 tumores de mama caninos (TCC) diagnosticados mediante análisis histopatológico para encontrar su relación con la neoplasia y la malignidad. IHC y RT-PCR se realizaron en tejidos CBT. La prueba de Fisher se utilizó para analizar la relación de WT1 con la malignidad. De los 15 tumores, 9 (60 %) fueron diagnosticados como benignos y 6 (40 %) fueron malignos. Con IHC, la expresión de WT1 fue positiva solo en biopsias diagnosticadas como malignas. La expresión de WT1 por RT-PCR se detectó en 14 de los 15 tumores (93,33 %), así como en el control de la glándula mamaria sana. Importancia clínica: este estudio describe por primera vez una estrecha correlación entre la TCC y un resultado positivo para la expresión de WT1 con IHC; por lo tanto, se puede utilizar como un biomarcador para esta neoplasia y como un indicador de malignidad. El análisis por RT-PCR también demostró ser una buena opción para detectar la expresión de WT1. Estos resultados serán útiles para futuras investigaciones para dilucidar las vías de señalización relacionadas con WT1 en la TCC. También para conocer moléculas que regulan la traducción de esta proteína como marcador de progresión tumoral.
Descritores: Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Genes do Tumor de Wilms/fisiologia
-Oncogenes
Imuno-Histoquímica
Biomarcadores Tumorais/metabolismo
Reação em Cadeia da Polimerase
Carcinogênese
Limites: Animais
Feminino
Cães
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1013933
Autor: Oliveros, Ricardo; Pinilla, Raúl E; Facundo Navia, Helena; Sánchez Pedraza, Ricardo.
Título: Cáncer gástrico: una enfermedad prevenible. Estrategias para intervención en la historia natural / Gastric cancer is a preventable disease: Strategies for intervention in its natural history
Fonte: Rev. colomb. gastroenterol;34(2):177-189, abr.-jun. 2019. tab, graf.
Idioma: es.
Resumo: Resumen El cáncer gástrico es un problema de salud pública. Las cifras de mortalidad y supervivencia son impresentables en nuestro país. En Colombia no existe ningún programa ni estrategias de diagnóstico temprano, ni tampoco es priorizado como un problema de salud. Los trabajos existentes demuestran que la mayoría de los pacientes cuando son diagnosticados presentan estadios avanzados. Un 90 % de los canceres gástricos se consideran consecuencia de un largo proceso inflamatorio sobre la mucosa gástrica. La infección por Helicobacter pylori es la principal etiología de la gastritis, la cual puede progresar a atrofia, metaplasia, displasia y cáncer. La atrofia gástrica establece un campo de cancerización más propenso a cambios moleculares y fenotípicos que terminan en un cáncer en crecimiento. Es claro que la historia natural proporciona un racional entendimiento clínico patológico para estrategias de prevención primaria y secundaria. Una evidencia bien establecida demuestra que la combinación de las estrategias primarias (erradicación del H. pylori) y secundarias (diagnóstico y seguimiento endoscópico de lesiones premalignas) pueden prevenir o limitar la progresión de la carcinogénesis gástrica. El riesgo de cáncer gástrico asociado con la gastritis por H. pylori puede ser estratificado de acuerdo con la gravedad y extensión de la atrofia de la mucosa gástrica. Esta aproximación está adaptada a diferentes países, de acuerdo con su incidencia específica de cáncer gástrico, condición socioeconómica y factores culturales, que requiere de la participación complementaria de los gastroenterólogos, los cirujanos, los oncólogos y patólogos. Frente a este problema de salud pública no hay ninguna acción por parte de las autoridades de salud ni del gremio médico. Por tanto, se revisan las estrategias de manejo que permitan intervenir la historia natural de la enfermedad con el objetivo de disminuir la incidencia y mortalidad. La implementación y estandarización de estas estrategias de manejo en nuestro medio podrán beneficiar a los pacientes con riesgo incrementado para cáncer gástrico y pueden implementarse (en países sin programas de tamizaje) de una forma racional, similar a como se está haciendo con el cáncer colorrectal, en todo el mundo.

Abstract Gastric cancer is a public health problem, but there are no usable mortality and survival statistics for Colombia. The country has no early diagnosis program or strategy, and gastric cancer is not prioritized as a health problem. Existing studies show that most patients are in advanced stages by the time they are diagnosed. Ninety percent of gastric cancers are considered to be consequences of long inflammatory processes in the gastric mucosa. H Pylori infections are the most common etiology of gastritis which can progress to atrophy, metaplasia, dysplasia and cancer. Gastric atrophy establishes a cancerization field which is prone to molecular and phenotypic changes that end in cancerous growth. It is well understood that a disease's natural history provides a rational pathological clinical understanding for primary and secondary prevention strategies. Well-established evidence shows that the combination of primary (H pylori eradication) and secondary strategies (diagnosis and endoscopic follow-up of pre-malignant lesions) can prevent or limit the progression of gastric carcinogenesis. The risk of gastric cancer associated with H pylori gastritis can be stratified according to the severity and extent of atrophy of the gastric mucosa. This approach has been adapted to many different countries according to specific incidences of gastric cancer, socio-economic conditions and cultural factors. This requires the complementary participation of gastroenterologists, surgeons, oncologists and pathologists. In the face of this public health problem, there has been no action by health authorities or the medical association. For this reason, we have reviewed management strategies that allow intervening into the natural history of the disease to reduce its incidence and mortality rate. The implementation and standardization of these management strategies in our environment may benefit patients who are at high risk for gastric cancer. These strategies can be implemented in a rational way, similar to what is being done with rectal cancer, in countries without screening programs all over the world.
Descritores: Neoplasias Gástricas
História Natural das Doenças
Diagnóstico Precoce
Carcinogênese
-Prevenção Primária
Helicobacter pylori
Prevenção Secundária
Autoridades de Saúde
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CO354 - Sociedad Colombiana de Gastroenterología


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Id: biblio-952804
Autor: Marques, Marcia M; Evangelista, Adriane F; Macedo, Taciane; Vieira, René Aloisio da Costa; Scapulatempo-Neto, Cristovam; Reis, Rui M; Carvalho, André L; Silva, Ismael Dale Cotrim Guerreiro da.
Título: Expression of tumor suppressors miR-195 and let-7a as potential biomarkers of invasive breast cancer
Fonte: Clinics;73:e184, 2018. tab, graf.
Idioma: en.
Resumo: OBJECTIVE: MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at the posttranscriptional level. Some miRNAs, including let-7a and miR-195, have been described as tumor suppressors. However, the roles of these microRNAs in breast cancer progression remain controversial. The aim of this study is to evaluate miR-195 and let-7a expression as potential biomarkers of invasive breast cancer. METHODS: In the present study, 200 individuals were separated into three groups: (i) 72 women constituting the control group who were selected according to rigorous and well-established criteria; (ii) 56 patients with benign breast tumors; and (iii) 72 patients with malignant breast cancers of different clinical stages. The miR-195 and let-7a expression levels in serum were evaluated by real-time PCR. The results were assessed alone and in combination, and the analysis included an estimation of sensitivity and specificity in ROC curves. RESULTS: Compared with the benign and control groups, both microRNAs were downregulated in the malignant breast cancer patient group. Compared with the malignant group, the combination of both biomarkers in the control and benign groups showed good sensitivity and specificity in the serum with AUCs of 0.75 and 0.72, respectively. The biomarker combination for the control group versus the malignant group exhibited a better sensitivity and specificity than for the benign group versus the malignant group. CONCLUSION: These findings support the evidence that the analysis of miR-195 and let-7a can be used as a non-invasive biomarker for breast cancer detection.
Descritores: Neoplasias da Mama/sangue
MicroRNAs/sangue
-Valores de Referência
Neoplasias da Mama/patologia
Biomarcadores Tumorais/sangue
Estudos de Casos e Controles
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
Modelos Logísticos
Estudos Prospectivos
Fatores de Risco
Análise de Variância
Sensibilidade e Especificidade
Reação em Cadeia da Polimerase em Tempo Real
Carcinogênese/patologia
Invasividade Neoplásica
Estadiamento de Neoplasias
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: biblio-1089608
Autor: Kosciuczuk, Urszula; Knapp, Pawel; Lotowska-Cwiklewska, Anna Maria.
Título: Opioid-induced immunosuppression and carcinogenesis promotion theories create the newest trend in acute and chronic pain pharmacotherapy
Fonte: Clinics;75:e1554, 2020.
Idioma: en.
Resumo: Opioids are the main group of pharmacological agents used during the perioperative period and provide a sedative and analgesic component. The observations of opioid consumption in West Europe indicate that this group of drugs is widely used in chronic noncancer pain therapy. Nearly 20 years ago, the first publications indicating that opioids, as an element of perioperative pharmacotherapy in oncologic patients, increase the risk of tumor recurrence and affect further prognosis were presented. The actual publications suggest that there are multifactorial, complex mechanisms underlying the immunological impact and carcinogenesis promotion of opioids and that the intensity varies depending on the type of opioid. There are also questions about the immunosuppressive effects among patients receiving opioids in the treatment of chronic noncancer pain. The aim of the review article is to present information about the action of opioids on the immune system in carcinogenic settings and to define the clinical usefulness of this pharmacological phenomenon.
Descritores: Dor Crônica/tratamento farmacológico
Carcinogênese
Analgésicos Opioides/efeitos adversos
-Sistema Hipófise-Suprarrenal/efeitos dos fármacos
Estudos Retrospectivos
Tolerância a Medicamentos
Analgésicos Opioides/uso terapêutico
Sistema Hipotálamo-Hipofisário/efeitos dos fármacos
Transtornos Relacionados ao Uso de Opioides
Limites: Humanos
Masculino
Feminino
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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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: lil-365254
Autor: Fett-Conte, Agnes C; Salles, Andréa B. C. F.
Título: A importância do gene p53 na carcinogênese humana / The importance of the p53 gene in human carcinogenesis
Fonte: Rev. bras. hematol. hemoter;24(2):85-89, abr.-jun. 2002.
Idioma: pt.
Resumo: Existem várias razões que justificam o título de "guardião do genoma" do gene P53. Seu envolvimento, direto ou indireto, tem sido observado na etiopatogenia de praticamente todas as neoplasias humanas, incluindo as leucemias e linfomas. Conhecer seus mecanismos de ação é fundamental para compreender os aspectos moleculares da carcinogênese. O presente trabalho apresenta uma revisão sobre as características deste gene e sua importância no diagnóstico, prognóstico e terapêutica, o que faz dele um alvo em potencial das estratégias de terapia gênica.
Descritores: Genes p53
-Terapêutica
Terapia Genética
Leucemia
Genoma
Diagnóstico
Carcinogênese
Neoplasias
Responsável: BR408.1 - Biblioteca da Faculdade de Medicina - BFM


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Id: biblio-1131890
Autor: Wang, Bingqi; Li, Xianping; Liu, Lei; Wang, Min.
Título: ß-Catenin: oncogenic role and therapeutic target in cervical cancer
Fonte: Biol. Res;53:33, 2020. tab, graf.
Idioma: en.
Projeto: Natural Science Foundation of Hunan Province.
Resumo: Cervical cancer is a common and fatal malignancy of the female reproductive system. Human papillomavirus (HPV) is the primary causal agent for cervical cancer, but HPV infection alone is insufficient to cause the disease. Actually, most HPV infections are sub-clinical and cleared spontaneously by the host immune system; very few persist and eventually develop into cervical cancer. Therefore, other host or environmental alterations could also contribute to the malignant phenotype. One of the candidate co-factors is the ß-catenin protein, a pivotal component of the Wnt/ß-catenin signaling pathway. ß-Catenin mainly implicates two major cellular activities: cell-cell adhesion and signal transduction. Recent studies have indicated that an imbalance in the structural and signaling properties of ß-catenin leads to various cancers, such as cervical cancer. In this review, we will systematically summarize the role of ß-catenin in cervical cancer and provide new insights into therapeutic strategies.
Descritores: Neoplasias do Colo do Útero/patologia
Infecções por Papillomavirus/patologia
beta Catenina/fisiologia
Via de Sinalização Wnt
Carcinogênese
Limites: Humanos
Feminino
Tipo de Publ: Revisão
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



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