Дисертації з теми "Melanoma cell proliferation"
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Ortega, Rose Mara 1974. "Análise dos mecanismos antiproliferativos decorrentes da inibição farmacológica da enzima ácido graxo sintase em células de melanoma murino B16-F10 : resultados in vitro e in vivo." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/289497.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: Ácido graxo sintase (FASN - fatty acid synthase, EC 2.3.1.85) é a enzima metabólica responsável pela síntese endógena do ácido graxo saturado palmitato, a partir dos precursores acetil-CoA e malonil-CoA. Diversos estudos mostram que, em contraste com a maioria das células normais, FASN é altamente expressa em vários tipos de neoplasias malignas humanas, tais como as de próstata, mama e melanoma sendo que, em alguns destes tumores, a alta expressão de FASN está associada a um pior prognóstico. A inibição da enzima FASN resulta em inibição da proliferação e induz morte celular em diversas neoplasias malignas. Recentemente demonstramos que, in vitro, a inibição específica da atividade de FASN em linhagem celular de melanoma murino, B16-F10, induz a via intrínseca da apoptose, com liberação de citocromo c e ativação de caspase-3, assim como altera a composição dos ácidos graxos livres presentes nas mitocôndrias das células B16-F10. O objetivo deste trabalho foi investigar de que maneira a inibição farmacológica de FASN reduz a proliferação de células B16-F10, in vitro e in vivo, utilizando C75 como inibidor de FASN. O tratamento de células e animais com C75 reduziu significativamente a proliferação celular e induziu apoptose. Houve significativa redução de células na fase S do ciclo celular, com acúmulo de células de G0/G1, em comparação com os controles. Western blottings feitos a partir de extratos de células em cultura e de tumores intraperitoneais mostraram aumento de p21WAF1/Cip1, p27Kip1, redução de Skp2 e cdk2, sem mudanças nos níveis de cdk4, 6 e ciclina E após tratamento com C75. A especifidade destes resultados foi confirmada pela redução da atividade enzimática de FASN após tratamento com C75 e pelo silenciamento de FASN com RNAi. Efeito anti-tumoral de C75 foi sugerido pela formação de tumores subcutâneos de menor volume quando comparados aos tumores de animais controle. Nossos achados mostram que a proliferação de células de melanoma é dependente de FASN, e que sua inibição primeiramente altera os níveis de proteínas envolvidas na transição de G1 para S, para posteriormente induzir apoptose em células de melanoma B16-F10
Abstract: Fatty acid synthase (FASN) is the metabolic enzyme responsible for the endogenous synthesis of the saturated long-chain fatty acid palmitate, from the precursors acetyl-CoA and malonyl-CoA. In contrast to most normal cells, the overexpression of FASN in several human malignancies, such as those of prostate, breast, ovary, melanoma, and soft tissue sarcomas has been associated with poor prognosis. FASN inhibition reduces cell proliferation by blocking DNA replication during S-phase, and induces apoptosis in several malignant neoplasias. We have previously shown that the specific inhibition of FASN activity significantly reduce proliferation and promote apoptosis, as demonstrated by the cytochrome c release and caspase-9 and -3 activation, as well as induces signi?cant changes in the free fatty acids composition of B16-F10 cells mitochondria. Here we investigated the events involved in cell cycle arrest subsequent to FASN inhibition with C75. C75 treatment significantly reduced melanoma cells proliferation and induced apoptosis in vitro and in mice. Cell cycle arrest after C75 treatment was evidenced by a significant increase in G0/G1 phase, as well as decline of the S phase, in comparison with untreated cells. Western blotting analysis showed significant accumulations of the tumor suppressor proteins p21WAF1/Cip1 and p27Kip1, together with decreased amounts of Skp2, essential for the proteasomal degradation of p27Kip1, and cdk2, a Ser/Thr protein kinase necessary for the G1/S transition, in C75-treated cells or mice tumors. The levels of other proteins involved in G1/S cell cycle progression, such as cyclin E, cdk4, and cdk6 were not affected by FASN inhibition. These results were confirmed by inhibition of FASN activity after C75 treatment and by RNAi for FASN. Antitumoral effect of C75 was suggested by reduced subcutaneous tumors volume when compared to controls mice. Our results suggest that melanoma murine B16-F10 cells proliferation is dependent on FASN activity, and its inhibition first modify the levels of some proteins involved in the transition G1?S of cell cycle, to finally induce apoptosis in neoplasic cells
Doutorado
Estomatologia
Doutora em Estomatopatologia
Haridas, Parvathi. "In vitro characterisation of melanoma progression in a melanoma skin equivalent model." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/118574/1/Parvathi_Haridas_Thesis.pdf.
Повний текст джерелаSIPES, NANCY JO. "GROWTH REGULATION OF HUMAN MELANOMA: FACTORS INVOLVED IN THE EXPRESSION OF THE TRANSFORMED PHENOTYPE (SOFT AGAR, GROWTH FACTORS, PLATELETS, ENDOTHELIAL CELLS, PARACRINE)." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183788.
Повний текст джерелаPetti, Carlotta. "Identification of molecular targets of oncogenic NRAs and BRAF involved in regulation of melanoma cell proliferation." Thesis, Open University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437808.
Повний текст джерелаStacy, Andrew Jared. "Regulation of ΔNp63α by TIP60 promotes cellular proliferation". Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1596151919161674.
Повний текст джерелаThieme, Sebastian, Sabine Stopp, Martin Bornhäuser, Fernando Ugarte, Manja Wobus, Matthias Kuhn, and Sebastian Brenner. "Expression of the melanoma cell adhesion molecule in human mesenchymal stromal cells regulates proliferation, differentiation, and maintenance of hematopoietic stem and progenitor cells." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-178636.
Повний текст джерелаThieme, Sebastian, Sabine Stopp, Martin Bornhäuser, Fernando Ugarte, Manja Wobus, Matthias Kuhn, and Sebastian Brenner. "Expression of the melanoma cell adhesion molecule in human mesenchymal stromal cells regulates proliferation, differentiation, and maintenance of hematopoietic stem and progenitor cells." Ferrata Storti Foundation, 2013. https://tud.qucosa.de/id/qucosa%3A28908.
Повний текст джерелаCardim, Sílvia Guedes Braga. "Vesículas extracelulares liberadas pelas células cancerosas modulam a proliferação, morte e migração celular no melanoma humano?" Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-15122017-083004/.
Повний текст джерелаTumor cells can interact with each other by releasing and incorporating extracellular vesicles, contributing to tumor progression. Therefore, the aim of this study was to evaluate if extracellular vesicles, such as microvesicles and exossomes, released by cancer cells under cell stress conditions like chemotherapy and hypoxia, induce an adaptive advantage to tumor cells. Our results show that vesicles shed by human melanoma cells under hypoxia, or normoxia exhibit the characteristic size of exossomes and microvesicles and do not modulate cell proliferation, death or migration. The vesicles released by melanoma cells after temozolomide treatment also showed the average size of exossomes and microvesicles; moreover, temozolomide treatment induced an increase in extracellular vesicles shedding by tumor cells. Incubation of tumor cells with vesicles released under temozolamide therapeutics caused an increase in cell proliferation, providing a proliferative advantage to human melanoma cells
Huang, Jie Min. "An amentoflavone derivative induces apoptosis and interferes with cell proliferation in melanoma by inhibition of the JAK2STAT3 signaling pathway." Thesis, University of Macau, 2017. http://umaclib3.umac.mo/record=b3690910.
Повний текст джерелаAbrantes, Julia Laura Fernandes 1984. "Expressão ectópica de miR-34a em células de melanoma metastático humano = efeitos sobre vias de sinalização relacionadas com sobrevivência, proliferação e morte celular = Ectopic expression of miR-34a in human metastatic melanoma cells: effects on signaling pathways related to survival, proliferation and cell death." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314040.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: O melanoma é o tipo mais agressivo de câncer de pele. Seu tratamento permanece como um grande desafio, já que em estágio avançado torna-se extremamente refratário aos tratamentos convencionais. miR-34a é um microRNA supressor de tumor com expressão normalmente reduzida em células cancerosas. A fim de investigar o papel de miR-34a como supressor do melanoma, o principal objetivo deste estudo foi identificar alvos moleculares modulados pela expressão ectópica de miR-34a na linhagem celular de melanoma metastático humano SK-mel-103. miR-34a reduziu significativamente a viabilidade das células de melanoma, o que deve estar relacionado, pelo menos em parte, com o aumento na expressão da proteína pró-apoptótica Bax, ativação da caspase-3 e clivagem da PARP-1. Estes dados sugerem que miR-34a foi capaz de induzir apoptose nas células de melanoma. Além disso, houve redução na expressão de CDK4, CDK6, E2F3 e pRb, proteínas relacionadas com a progressão do ciclo celular. Aumento na expressão de p21, um inibidor de CDKs, também foi observado nessas células. Algumas moléculaschave envolvidas com os processos de proliferação celular e apoptose, como proteínas oncogênicas (Axl, AKT, ERK 1/2, ?-catenina e c-myc) e proteínas supressoras de tumor (p53 e PTEN), foram "down- e upreguladas" por miR-34a, respectivamente. Interessantemente, o fluxo autofágico foi aumentado por miR-34a, efeito que não foi correlacionado com alterações adicionais na viabilidade das células de melanoma. O aumento no fluxo autofágico ocorreu, provavelmente, como uma resposta celular ao estresse de retículo e a agregação de proteínas induzidos por miR-34a, fenômenos que também podem ter contribuído para a indução de apoptose nesse contexto. Os dados obtidos neste estudo trouxeram novos aspectos moleculares da ação de miR-34a como supressor tumoral, e permitem apontar este microRNA como um potencial alvo terapêutico contra o melanoma metastático humano
Abstract: Melanoma is the most aggressive form of skin cancer. Its treatment remains a big challenge, since in advanced stage it is extremely refractory to conventional treatments. miR-34a has emerged as an important tumor suppressor, and its expression is normally reduced in cancer cells. To provide more information about the role of miR-34a as a melanoma suppressor, the main goal of this study was to identify key molecular players modulated by ectopic expression of this microRNA in the metastatic melanoma cell line SK-mel-103. miR-34a caused a reduction of melanoma cells viability, what may be related, at least in part, with the increased expression of pro-apoptotic marker, Bax, activation of caspase 3 and PARP-1 cleavage, which indicates that miR-34a triggered apoptosis in melanoma cells. In addition, the expression of CDK4, CDK6, E2F3 and pRb, proteins related to the cell cycle progression, was reduced. An increase in p21 expression, a CDK inhibitor, was also detected in these cells. Some key molecules involved with proliferation and apoptosis processes, such as oncogenic proteins (Axl, AKT, ERK 1/2 kinases, ?- catenin and c-myc) and tumor suppressor proteins (p53 and PTEN), were down- and upregulated by miR-34a, respectively. Interestingly, the autophagic flux was stimulated by miR-34a, but this effect was not correlated with further alterations in cell viability. The increased autophagy occurred probably as a cellular response against the reticulum stress and the protein aggregation induced by miR-34a in melanoma cells, which can also be contributing to the cell death by apoptosis in this context. Our findings brought up novel molecular aspects about the role of miR-34a as melanoma suppressor. The broad action of this microRNA on key molecular players of melanoma aggressiveness was crucial for reprogramming these cells in favor of apoptosis. Altogether, this study pointed out miR-34a as a potential therapeutic agent against advanced melanoma
Doutorado
Bioquimica
Doutora em Biologia Funcional e Molecular
Passos, Luis Augusto Abreu da Cunha. "A sinalização do co-ativador de transcrição PGC-1beta e sua relevância para a proliferação celular e desenvolvimento de melanoma." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-31032015-162021/.
Повний текст джерелаPGC-1beta is a co-activator of gene transcription primarily responsible for the regulation of cellular metabolism, mainly in mitochondrial biogenesis and function and also substrate and lipid synthesis. In recent years, other isoforms of PGC-1 have been described as participating in the genesis and maintenance of tumors. Therefore, our objective was to determine whether PGC-1beta is related to increased proliferation of melanoma cells. Initially, it was demonstrated that mRNA and protein levels of PGC-1beta are much higher in melanoma cell lines (Tm1 and TM5) than in the non-tumoral parental lineage melanocytes (melan-a) as detected by quantitative PCR and Western blotting. In order to find a causal relationship between the expression of PGC-1beta and cell growth, Tm5 lineage cells were transfected with an antisense oligonucleotide (ASO) against PGC-1beta. The cells treated with ASO had lower levels of PGC-1beta mRNA and protein, as well as reduction in its activity detected by quantitation of PGC-1beta dependent genes expression. Furthermore, transfected cells showed a lower rate of proliferation compared to Tm5control cells. This phenomenon was also observed in vivo. When injected into mice, Tm5 cells develop a tumor which reaches 1.34 ± 0.20 cm3 after nine days. Tumors treated with ASO, after the same time, presented tumor volume of 0.75 ± 0.05 cm 3. This growth was not related to tumor necrosis, but with reduced cell proliferation. Finally, we checked whether the same phenomenon would be observed in humans. The PGC-1beta expression was much higher in melanoma samples than in nevi, a non-malignant skin alteration filled with melanin. Therefore, we concluded that PGC-1beta expression in melanoma is increased, both in murine and human, and that blocking its activity leads to decreased cell proliferation and tumor growth
Azevedo, Ricardo Alexandre de. "Avaliação da atividade proliferativa, antitumoral e hematológica dos peptídeos derivados da caseína INKKI e YPVEPFTE no melanoma experimental." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-14082009-093334/.
Повний текст джерелаPeptides INKKI and YPVQPFTE were isolated from the bovine b-casein after hydrolysis corresponding to the 23-30 and 114-121 sequence, respectively. Evaluation of the proliferative activity in primary cultures of lymphocytes. The activity antitumor in vitro was accomplished culture of was studied. Groups with 40 C57BL/6J lines mice had been used to evaluate the antitumoral activity. Our results showed that peptide presented similar proliferative response to the PHA commercial mitogen. The peptide YPVEPFTE showed to have proliferative action larger than presented by the commercial mitogen. The peptide INKKI showed in the chemotactic action. The treatment in vitro had shows that the peptide INKKI induces selective citotoxicity. The bearing animals of dorsal tumors had presented significant inhibition of the capacity of growth and the spread of methastasis. Thus, the peptides casein present significant action in in vitro and in vivo experiments, suggesting a possible physiologic role.
Vo, Brenda. "Novel likelihood-free Bayesian parameter estimation methods for stochastic models of collective cell spreading." Thesis, Queensland University of Technology, 2016. https://eprints.qut.edu.au/99588/1/Brenda_Vo_Thesis.pdf.
Повний текст джерелаLautenschlager, Willian Wagner. "Um modelo estocástico de simulação da dinâmica dos queratinócitos, melanócitos e melanomas no desenvolvimento dos tumores." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/100/100132/tde-21082017-174520/.
Повний текст джерелаDuring the last decades, tumor biology research with the use of new techniques in molecular biology resulted in a profusion of information that have given conditions and motivated the development of new mathematical models dedicated to analyzing various aspects of growth and proliferation of the cell population. Some of these models have been devoted to the description and analysis of the steady state of the development process of a cell population under chemical conditions that, in theory, promote the acceleration or deceleration of the growth of tumor cell population. However, these studies have not yet analyzed the temporal dynamics of growth of a tumor cell population. One of the difficulties is the establishment of the interaction between cells of multiple types that serve as the description for this dynamic. Our work fills this gap and this dissertation aims to present the model, developed by us, to simulate the growth dynamics and cellular proliferation of melanoma (cancer of low incidence but of extremely high lethality) and the results obtained through the simulations of this computational model
Fedele, Thiago Antonio. "Análise metabolômica de animais portadores de melanoma murino B16F10 por espectroscopia de ressonância magnética nuclear (RMN)." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-22012013-165318/.
Повний текст джерелаThe metabolome is defined as the qualitative and quantitative collection of all low weight molecular metabolites in cells that participate in biochemical reactions necessary for the maintenance, growth and physiology of cell. The metabolomic evaluation allows the design of systems of biochemical process in order to broaden the understanding of how diseases manifest. The Nuclear Magnetic Resonance Spectroscopy (NMR) is used for investigating a variety of biological processes in several systems. The magnetics applied to cell and tissue biopsies intact murine melanoma B16F10 contributed to the biochemical characterization of biomarkers of different stages of tumor progression of murine melanoma B16F10. The results obtained in this study allowed the identification of 33 potential metabolites involved in lipid content in the secondary metabolism of the glycolytic pathway, which promote growth and tumor progression. The presence of taurine, proline, serine, phenylalanine, which quantitatively increased, is possibly markers of invasion and metastasis progression. Quantitative analysis of these metabolites showed a significant difference in 11 compounds, of which 9 are directly involved in the expression of proliferative responses, cell death and angiogenesis in different periods of growth of B16F10 melanoma, evaluated in this study. Thus, the findings from this study, when associated in the future with other factors, may be useful in the diagnosis and may assist in choosing therapeutic target with greater specificity and fewer side effects. NMR may have a significant impact on monitoring metabolites in tumor cells and tissues, allowing for earlier detection of malignant tumors; in short, by combining MRI methods.
Oliveira, Maria Theresa de [UNIFESP]. "O uso de interferência por RNA para a análise da função do gene E2F1 na progressão do ciclo celular em células tumorais." Universidade Federal de São Paulo (UNIFESP), 2010. http://repositorio.unifesp.br/handle/11600/9874.
Повний текст джерелаE2F1 pertence a uma família de fatores de transcrição e possui papel central no controle da expressão de genes relacionados à regulação da proliferação celular, pois ativa genes que participam da síntese de DNA. A atividade de E2F1 é regulada por meio da proteína pRB que, quando fosforilada por quinases associadas à ciclinas (Ciclinas/CDK) libera este fator de transcrição, promovendo assim a proliferação. A disfunção da complexa via de regulação da divisão celular pode acarretar em proliferação exacerbada, sendo a superexpressão de E2F1 bastante comum em diferentes tipos de tumores. Este fenômeno pode ser o principal fator para a alta proliferação de células tumorais. Desta forma, a inibição da atividade de E2F1 através de RNA de interferência (RNAi) pode ser promissora como tratamento para a diminuição da proliferação de células de melanoma. Assim sendo, objetiva-se neste trabalho inativar por RNAi o gene E2f1 em células B16mCAR, derivadas de melanoma de C57BL/6 e que superexpressam o receptor CAR, e averiguar os efeitos de sua ausência na proliferação celular, tanto in vitro como in vivo.
E2F1 belongs to a family of transcription factors and plays a central role in controlling the expression of genes related to regulation of the cell-cycle progression, since it activates genes involved in DNA synthesis. The activity of E2F1 is regulated by pRB protein, that when phosphorylated by cyclin-dependent kinases cyclins (Cyclins/CDK) releases this transcription factor, thereby promoting proliferation. The dysfunction of the complex regulatory pathway of cell division can lead to excessive proliferation, which overexpression of E2F1 is quite common in different types of tumors. This phenomenon may be the main factor for the high proliferation of tumor cells. Thus, inhibition of E2F1 activity by RNA interference (RNAi) may be promising as a treatment for decreased proliferation of melanoma cells. Therefore, the purpose of this work is the inactivation of the E2f1 gene through RNAi in B16mCAR cells, derived from C57BL/6’s melanoma and overexpresses the CAR receptor, and also verifies the effects of its absence on cell proliferation in vitro and in vivo.
TEDE
BV UNIFESP: Teses e dissertações
Morales, Delphine. "Modèles 3D de mélanome métastatique pour l’évaluation in vitro de l’efficacité de molécules de thérapies ciblées." Thesis, Compiègne, 2019. http://www.theses.fr/2019COMP2498.
Повний текст джерелаMelanoma cell sensitivity to targeted therapy molecules is dependent on the tumor microenvironment (cell-cell and cell-extracellular matrix interactions). Three dimensional (3D) in vitro cell culture systems better reflect the native structural architecture of tissues and are attractive to investigate cellular interactions. We have developed and compared several metastatic melanoma models: melanoma cells (SK-MEL-28 and SK-MEL-3, BRAF V600E mutant and SK-MEL-2 BRAF wt) cultured as a monolayer (2D) and co-cultured on 3D dermal equivalents with fibroblasts to better unravel factors modulating cell sensitivity to a BRAF inhibitor (BRAFi, Vemurafenib) and a BRAFi combined with a MEK inhibitor (MEKi, Cobimetinib). Cell sensitivity to treatments was evaluated under various aspects: cell proliferation (cell counting, EdU incorporation, MTS assay), MAPK and PKB/Akt signaling pathway analysis (Western-blotting), apoptosis (TUNEL), cytokine and growth factor release (ELISA) and histology (3D models). A cytostatic effect of BRAFi was observed on SK-MEL-28 and SK-MEL-3 cells in both models. SK-MEL-2 cell line was clearly resistant to BRAFi when cultured as a monolayer but not when co-cultured with 3D fibroblasts embedded in a type I collagen matrix. Conditioned media provided by 3D fibroblasts (dermal equivalents) underlined 2D SK-MEL-2 sensitivity to BRAFi. Cell culture supernatant analysis revealed that dermal equivalents released some soluble factors (IL-6, IL-8, HGF, TGF-β): these secretions were modified during vemurafenib treatment. The combination of treatment with MEKi enhances the action of Vemurafenib on metastatic melanoma cells while decreasing the proliferation capacity of fibroblasts. Cell populations containing melanoma cells or fibroblasts associated with cancer (CAFs) were isolated from a cutaneous metastasis biopsy of a patient with metastatic melanoma. These cells allowed the realization of patient-specific models of metastatic melanoma in order to study in vitro the sensitivity of the patient’s melanoma cells to treatments in a tumor microenvironment (paracrine secretion of stromal cells and collagen matrix). These 3D predictive patient-specific models could be used to determine personalized therapy strategies, as well as to understand the resistance phenomena of melanoma cells to treatments
RODRIGUES, DANIELLE B. "Terapia antiangiogênica de tumores utilizando células produtoras de endostatina encapsuladas em sipositivos de imunoisolamento." reponame:Repositório Institucional do IPEN, 2008. http://repositorio.ipen.br:8080/xmlui/handle/123456789/11711.
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Dissertacao (Mestrado)
IPEN/D
Instituto de Pesquisas Energeticas e Nucleares - IPEN/CNEN-SP
Marshall, Jean-Claude. "The proliferative and invasive capabilities of five human uveal melanoma cell lines /." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82296.
Повний текст джерелаOur laboratory utilizes five human uveal melanoma cell lines (92.1, MKT-BR, OCM-1, SP-6.5, UW-1) that have a previously described metastatic potential from an animal model (MP). We used four methods to characterize the proliferation rate of these five cell lines. We also used a Matrigel invasion assay to assess the invasive ability of the same cell lines in response to the potential chemo-attractants: interleukin-6, Vascular Endothelial Growth Factor, and Fetal Bovine Serum.
From these results we were able to propose a novel classification system for our cell lines: high proliferation and high invasion/high MP, low proliferation and low invasion/low MP, and high proliferation and invasion/no MP.
From these results we were able to propose a novel classification system for our cell lines: high proliferation and high invasion/high MP, low proliferation and low invasion/low MP, and high proliferation and invasion/no MP.
Andrade, Bruno Augusto Benevenuto de 1984. "Immunohistochemical analysis of the expression of FASN and proteins associated with proliferation and cell cycle control in melanocytic nevi and primary oral melanomas = Análise imunoistoquímica da expressão de FASN e de proteínas associadas à proliferação e controle do ciclo celular em nevos melanocíticos e melanomas primários de boca." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/288360.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: O melanoma bucal é um tumor potencialmente agressivo de origem melanocítica, que surge através de uma lesão melanocítica benigna ou de melanócitos da mucosa. Em melanomas é conhecido que a transformação de melanócitos em células de melanoma decorre de alterações nos mecanismos de controle do ciclo celular. Nesse caso, as alterações mais comuns são a superexpressão de ciclina D1e Skp2 e mutações ou deleções de p16, p21 e p27. A avaliação do ciclo celular usando anticorpos contra proteínas nucleares envolvidas na regulação da replicação de DNA também ganhou interesse especial na tentativa de predizer o comportamento biológico em tumores malignos e diferenciação entre lesões benignas e malignas. O objetivo desse trabalho foi avaliar a expressão imunoistoquímica de ácido graxo sintase (FASN) e de proteínas envolvidas nos mecanismos de controle e progressão do ciclo celular como p16, p21, p27, ciclina D1 e Skp2, além dos marcadores de proliferação celular Mcm-2, Ki-67 e geminina em nevos intramucosos e melanomas primários de boca. Os resultados mostraram que FASN, p21, ciclina D1, Skp2, Ki-67, Mcm-2 e geminina foram negativos ou raramente expressos nos casos de nevo, enquanto que nos casos de melanoma, observou-se alta expressão dessas proteínas. Esses marcadores podem estar envolvidos na patogênese do melanoma bucal, podendo eventualmente ser utilizados como ferramenta diagnóstica adicional para ajudar no diagnóstico diferencial entre lesões melanocíticas benignas e malignas
Abstract: Oral melanoma is a potentially aggressive tumor of melanocytic origin, which arises from a benign melanocytic lesion or mucosal melanocytes. In melanomas it is known that the transformation of melanocytes in melanoma cells is caused by alterations in the mechanisms of cell cycle control. In this case, the most common changes are the overexpression of cyclin D1 and Skp2 and mutations or deletions of p16, p21 and p27. The evaluation of the cell cycle using antibodies against nuclear proteins involved in the regulation of DNA replication has also gained particular interest in the effort to predict the biologic behavior and to differentiate between benign and malignant lesions. The aim of this study was to evaluate the immunohistochemical expression of fatty acid synthase (FASN) and proteins involved in the mechanisms of control and cell cycle progression such as p16, p21, p27, cyclin D1 and Spk2, and the cell proliferation markers Mcm-2, Ki-67 and geminin in intramucosal nevi and oral primary melanomas. The results showed that FASN, p21, cyclin D1, Skp2, Ki-67, MCM-2 and geminin were negative or rarely expressed in the cases of nevi, whereas in the cases of melanoma, it was observed a high expression of these proteins. These markers may be involved in the pathogenesis of oral melanoma and may eventually be used as additional diagnostic tool to help in the differential diagnosis between benign and malignant melanocytic lesions
Doutorado
Patologia
Doutor em Estomatopatologia
Cheng, Shu-Wei, та 鄭舒薇. "β2-glycoprotein I inhibits melanoma cell proliferation, migration and invasion through its functional domain". Thesis, 2016. http://ndltd.ncl.edu.tw/handle/est792.
Повний текст джерела國立陽明大學
生化暨分子生物研究所
104
Abstract β2-glycoprotein I (β2-GPI), which consists of five homologous domains, is a human plasma glycoprotein with diverse pathophysiological functions. In our previous study, β2-GPI could suppress vascular endothelial growth factor-induced human aortic endothelial cell proliferation, migration and angiogenesis. Angiogenesis is essential for tumor progression; however, the effects of β2-GPI on tumor cell proliferation, migration and invasion remain unclear. We were also interested in elucidating the correlation between the structural features of β2-GPI and their anti-tumor function. Thus, the aim of this study was to investigate the functional domain ofβ2-GPI which plays a role in anti-tumor cell proliferation, migration, invasion and its molecular mechanisms. Using cell counting assays, we found that purified β2-GPI from human plasma and recombinant peptides of different β2-GPI domains, including domain I-V (DI-V), domain I-IV (DI-IV) and domain I (DI), inhibited B16-F10 melanoma cell proliferation but not domain IV (DIV) and domain V (DV) ofβ2-GPI. Purified 2-GPI and these recombinant peptides also inhibited B16-F10 cell migration by wound healing and transwell assays. Moreover, purified β2-GPI and these recombinant peptides suppressed B16-F10 cell invasion by invasion assay. These inhibitions were also achieved by recombinant peptides of β2-GPI-DI in a dose-dependent manner. In addition, purified β2-GPI and these recombinant peptides was found to reduce Akt and p38 phosphorylation and downregulate MMP-2 protein expression in B16-F10 cells by western blot analysis. Furthermore, we found that purified β2-GPI and the functional recombinant peptides inhibited tumor volume and tumor weight in the B16-F10-implanted C57BL/6 mice. Our results suggest that β2-GPI is able to inhibit B16-F10 cell proliferation, migration and invasion in vitro as well as tumor growth in vivo, which indicates a potential for clinical therapy of melanoma.
Swen, Shu Ping, and 孫淑萍. "The Effects of Low-Energy Helium-Neon Laser Irradiation on Migration and Proliferation in Human Melanoma cell lines." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/16418172493360860529.
Повний текст джерела高雄醫學大學
生物化學研究所
90
Abstract Helium-Neon laser can improve healing wound repair and regulation cell cycle .Those are associate with cell migration and cell proliferation .So , we are interesting in if He-Ne can influence cell migration and cell proliferation in human malignant melanoma cell lines. Cell migration is about cell cytoskeleton and cell membrane interaction and signal pathway to change cell shape and behavior on extracellular matrix to control cell survival , cell cytoskeleton reorganization, cell mobility and receptor activation Cell proliferation is a result from cell cycle , and cell cycle is a mother cell division to daughter cell pathway ,so , cell proliferation is association with increase cell proliferatic protein , DNA synthesis and cell number .Our study focus on (1)if He-Ne laser influence melanoma cell lines migration correlates with cell surface receptor signaling pathway.(2) if He-Ne laser influence melanoma cell lines cell proliferation .The results show when He-Ne laser irradiation dose is more than 0.5 J/cm2,can increase α3β1 integrin and P125FAK phosphorylation and F-actin stress fibers expression ,but no effect on cell damage and cell proliferation in A375 melanoma cell line .And when He-Ne laser irradiation dose is 1J/cm2~2 J/cm2,can increase expression Ki-67 proliferatic protein cell number and cell number after 72 hours ,but no effect on cell migration and cell damage in A2058 melanoma cell line .Our results support He-Ne laser can involve A375 melanoma cell line migration and increase A2058 melanoma cell line proliferation ,So ,we suggest He-Ne laser can effect on different bio-stimulation in different cells .
Nemazannikova, Natalie. "Vitamin D and non-melanoma skin cancer." Thesis, 2016. https://vuir.vu.edu.au/32150/.
Повний текст джерелаTzi-Peng and 楊子芃. "1.Mithramycin A inhibits human epithelial carcinoma cells 1.proliferation and migration involving downregulation of Eps8 expression 2.Mechanism of cell death induced by Caffeic acid on melanoma cells." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/99219699772727063271.
Повний текст джерела中山醫學大學
生化暨生物科技研究所
100
Part1 Mithramycin A is an inhibitor of the binding of the Sp family transcription factor to the GC box. Many studies show that Mithramycin A may reduce the expression of many proto-oncogenes by inhibiting the mRNA and protein synthesis and it has been used as an antibiotic chemotherapy drug for a long time. Recently, Eps8 (EGFR pathway substrate 8) has been revealed to be a novel proto-oncogene related to cellular transformation, Rac activation and actin barbed-end-capping activity. Therefore, the aim of this study was to verify whether Eps8 might be regulated by Mithramycin. Results showed that Mithramycin could reduce the mRNA and protein levels of Eps8 in dose- and time-dependent manners in several cancer cell lines. Furthermore, cell growth and migration ability were also reduced significantly by Mithramycin A treatment. Since Src is a well-known Eps8 activity enhancer, a v-Src transfected IV5 cell line was subjected to Mithramycin A treatment and then analyzed to show that Src expression was unable to restore the Mithramycin-induced decrease in Eps8 expression, cell growth, and migration ability. To further confirm the above mentioned results, the expression of Eps8 was eliminated by a transient transfection with siRNA and subsequent analysis showed that silencing of Eps8 might also lead to a reduced growth and migration ability of cancer cells. These findings suggested that Eps8 was involved in the regulation of growth and motility of cancer cells and Mithramycin A might exert its anticancer ability via a pathway involving the downregulation of Eps8. Part2 Caffeic acid is an organic compound found in plants which also shows antioxidant, immunomodulatory, antiinflammtory and antitumor activities. Melanoma is tumorigenesis of melanocytes which produce melanin in the skin or other organs. It has a bad prognosis and difficult to treat when tumor become malignant. Studies has showed some chemicals or drugs reduced the proliferation of melanoma cells through inducing autophagy. We treat the melanoma cell line B16-F1 with Caffeic acid and find that cells go autophagy and the cell mobility diminished. The autophagy regulators p-Akt is down-regulated, and p-AMPK is up-regulated. FASN (Fatty acid synthase), a tumor related protein which can be activated by Akt and inhibited by AMPK is decreased. Beclin-1 and LC3, the autophagy regulated proteins, are express increasd. For investigate the roles of AMPK, we block the phosphorylation of AMPK by Compound C. Results show the effects of growth and migration abilities inhibited by Caffeic acid was recovery. Autophagy related proteins Beclin-1 and LC3 was recovery partially. It means that AMPK is one of the key regulator intermediate with Caffeic acid induced autophagy. It is worthy for the prophylaxis of melanoma to comprehend the death mechanisms regulated in cells. Our study shows Caffeic acid, the antioxidant ingredients conclude commonly in the plants, inhibit the cell mobility and decrease the cell growth of B16-F1 cells through autophagy. This mechnism is regulated by Akt and AMPK. Although it need more investigates to realize the factors involved, we still get an active principle for tumor inhibition and it is important for chemoprevention of melanoma.
Kim, Edward. "P300 critically controls proliferation and survival of melanoma cells by transcriptionally regulating MITF." Thesis, 2017. https://hdl.handle.net/2144/27182.
Повний текст джерела2018-12-14T00:00:00Z
Hu, Wan-Ping, and 胡婉萍. "Study of Molecular Mechanisms in Helium-Neon Laser-induced Proliferation in Human Melanoma A2058 Cells." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/63476912342029661259.
Повний текст джерела高雄醫學大學
醫學研究所博士班
95
Previous reports have shown that cellular functions could be influenced by visual light (400 - 700 nm). Recent evidence indicates that cellular proliferation could be triggered by the interaction of helium-neon laser (He-Ne laser, 632.8 nm) with the mitochondrial photoacceptor-cytochrome c oxidase. Our previous studies demonstrated that He-Ne irradiation induced an increase in cell proliferation, but not migration, in the melanoma cell line A2058 cell. The aim of this study was to investigate the underlying mechanisms involved in photostimulatory effects induced by an He-Ne laser. Using the A2058 cell as a model for cell proliferation, the photobiologic effects induced by an He-Ne laser were studied. He-Ne irradiation immediately induced an increase in mitochondrial membrane potential (ΔΨmt), ATP, and cAMP via enhanced cytochrome c oxidase activity and promoted phosphorylation of Jun N-terminal kinase (JNK) / activator protein-1 (AP-1) expressions. He-Ne irradiation-induced A2058 cell proliferation was significantly abrogated by the addition of ΔΨmt and JNK inhibitors. Moreover, treatment with an He-Ne laser resulted in delayed effects on interleukin-8 (IL-8) and transforming growth factor-β1 (TGF-β1) release from A2058 cells. These results suggest that He-Ne irradiation elicites photostimulatory effects in mitochondria processes, which involve JNK/AP-1 activation and enhanced growth factor release, and ultimately lead to A2058 cell proliferation.