Добірка наукової літератури з теми "Melanoma cell proliferation"
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Статті в журналах з теми "Melanoma cell proliferation"
Schadendorf, D., A. Möller, B. Algermissen, M. Worm, M. Sticherling, and B. M. Czarnetzki. "IL-8 produced by human malignant melanoma cells in vitro is an essential autocrine growth factor." Journal of Immunology 151, no. 5 (September 1, 1993): 2667–75. http://dx.doi.org/10.4049/jimmunol.151.5.2667.
Повний текст джерелаChen, Xianjin, Lili Chang, Yan Qu, Jinning Liang, Waishu Jin, and Xiujuan Xia. "Tea polyphenols inhibit the proliferation, migration, and invasion of melanoma cells through the down-regulation of TLR4." International Journal of Immunopathology and Pharmacology 31 (January 1, 2018): 039463201773953. http://dx.doi.org/10.1177/0394632017739531.
Повний текст джерелаLa, Ting, Lei Jin, Xiao Ying Liu, Ze Hua Song, Margaret Farrelly, Yu Chen Feng, Xu Guang Yan, et al. "Cylindromatosis Is Required for Survival of a Subset of Melanoma Cells." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 28, no. 4 (September 1, 2020): 385–98. http://dx.doi.org/10.3727/096504020x15861709922491.
Повний текст джерелаKang, Wesuk, Dabin Choi, Soyoon Park, and Taesun Park. "Carvone Decreases Melanin Content by Inhibiting Melanoma Cell Proliferation via the Cyclic Adenosine Monophosphate (cAMP) Pathway." Molecules 25, no. 21 (November 7, 2020): 5191. http://dx.doi.org/10.3390/molecules25215191.
Повний текст джерелаWellbrock, Claudia, and Richard Marais. "Elevated expression of MITF counteracts B-RAF–stimulated melanocyte and melanoma cell proliferation." Journal of Cell Biology 170, no. 5 (August 29, 2005): 703–8. http://dx.doi.org/10.1083/jcb.200505059.
Повний текст джерелаTsai, Alexander, and Eduardo Davila. "A multikinase inhibitor and DNA-PK inhibitor combination reduces tumor growth and alters the tumor microenvironment of B16 melanoma." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 213.2. http://dx.doi.org/10.4049/jimmunol.196.supp.213.2.
Повний текст джерелаLucas, Lauren M., Vipasha Dwivedi, Rania H. Mohamedelhassan, Erin L. Harrell, Connor M. Kelley, Elizabeth L. Knerr, Jessica A. Markham, and David J. Riese. "Abstract 4000: ERBB4 is sufficient and necessary for proliferation of BRAF WT melanoma cell lines." Cancer Research 82, no. 12_Supplement (June 15, 2022): 4000. http://dx.doi.org/10.1158/1538-7445.am2022-4000.
Повний текст джерелаWang, Shu Jing, Jia Liu, Fei Wang, Ning Chen, Shan Jiang, Lin Liu, Ying Zhao, and Xiao Dan Zhang. "Tumstatin 7 Peptide Affect Biological Activity of B16 Melanoma Cell." Advanced Materials Research 641-642 (January 2013): 915–18. http://dx.doi.org/10.4028/www.scientific.net/amr.641-642.915.
Повний текст джерелаHenderson, Evita, and Curtis E. Margo. "Iris Melanoma." Archives of Pathology & Laboratory Medicine 132, no. 2 (February 1, 2008): 268–72. http://dx.doi.org/10.5858/2008-132-268-im.
Повний текст джерелаVital, Patrik da Silva, Murilo Bonatelli, Marina Pereira Dias, Larissa Vedovato Vilela de Salis, Mariana Tomazini Pinto, Fátima Baltazar, Silvya Stuchi Maria-Engler, and Céline Pinheiro. "3-Bromopyruvate Suppresses the Malignant Phenotype of Vemurafenib-Resistant Melanoma Cells." International Journal of Molecular Sciences 23, no. 24 (December 9, 2022): 15650. http://dx.doi.org/10.3390/ijms232415650.
Повний текст джерелаДисертації з теми "Melanoma cell proliferation"
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
Made available in DSpace on 2018-08-22T16:08:32Z (GMT). No. of bitstreams: 1 Abrantes_JuliaLauraFernandes_D.pdf: 4562084 bytes, checksum: fba9dbca16cd31c006b311ff23a0b41b (MD5) Previous issue date: 2013
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
Частини книг з теми "Melanoma cell proliferation"
Lozhkomoev, Aleksandr S., Georgy Mikhaylov, Vito Turk, Boris Turk, and Olga Vasiljeva. "Application of Crumpled Aluminum Hydroxide Nanostructures for Cancer Treatment." In Springer Tracts in Mechanical Engineering, 211–23. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-60124-9_10.
Повний текст джерелаKim, Yon-Suk, Sun Hee Cheong, Jin-Woo Hwang, Gaurav Lodhi, Kwang-Ho Lee, Dong-Kug Choi, Hyuk Song, et al. "Effect of Taurine on Viability and Proliferation of Murine Melanoma B16F10 Cells." In Taurine 9, 167–77. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15126-7_15.
Повний текст джерелаSchadendorf, D., M. Worm, K. Jurgovsky, E. Dippel, U. Reichert, and B. M. Czarnetzki. "Effects of Various Synthetic Retinoids on Proliferation and Immunophenotype of Human Melanoma Cells In Vitro." In Recent Results in Cancer Research, 183–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-78771-3_13.
Повний текст джерелаA., K., E. I., V. Yu., E. V., N. I., A. A., I. N., N. V., and H. M. "T-Cadherin Stimulates Melanoma Cell Proliferation and Mesenchymal Stromal Cell Recruitment, but Inhibits Angiogenesis in a Mouse Melanoma Model." In Research Directions in Tumor Angiogenesis. InTech, 2013. http://dx.doi.org/10.5772/53350.
Повний текст джерелаNguyen, Duy, Oanh Nguyen, Honglu Zhang, Glenn D., and Mandi M. "A Bromophosphonate Analogue of Lysophosphatidic Acid Surpasses Dacarbazine in Reducing Cell Proliferation and Viability of MeWo Melanoma Cells." In Research on Melanoma - A Glimpse into Current Directions and Future Trends. InTech, 2011. http://dx.doi.org/10.5772/18702.
Повний текст джерелаNordenberg, J., A. Fuchs, L. Wasserman, Z. Malik, and A. Novogrodsky. "Anti-proliferative effects and phenotypic alterations induced by methylurea derivatives in B16 mouse melanoma." In Modern Approaches to Animal Cell Technology, 125–37. Elsevier, 1987. http://dx.doi.org/10.1016/b978-0-408-02732-8.50016-x.
Повний текст джерелаТези доповідей конференцій з теми "Melanoma cell proliferation"
Ollinger, K., and P. Waster. "PO-158 Extracellular vesicles, generated from UVA-exposed melanoma cells, promotes cell proliferation and invasion." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.197.
Повний текст джерелаZhan, Yao, Michael S. Dahabieh, Filippa Pettersson, Monica C. Dobocan, Marie Noel M. Boutchou, Leon Van Kempen, Sonia V. del Rincon, and Wilson H. Miller. "Abstract 3710: The role of eIF4E in promoting melanoma cell proliferation and maintaining acquired resistance to Vemurafenib in melanoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3710.
Повний текст джерелаZhan, Yao, Michael S. Dahabieh, Sonia V. del Rincon, and Wilson H. Miller. "Abstract B235: The role of eIF4E in promoting melanoma cell proliferation and maintaining acquired resistance to vemurafenib in melanoma." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b235.
Повний текст джерелаSrivastava, Jaya, Okkyung Rho, and John DiGiovanni. "Abstract 2022: Twist1 regulates UVB-induced epidermal cell proliferation in non-melanoma skin cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2022.
Повний текст джерелаShen, Che-Hung, Ping Yuan, Rolando Perez-Lorenzo, Yaqing Zhang, Sze Xian Lee, Yang Ou, Li Cai, John M. Asara, Lewis C. Cantley, and Bin Zheng. "Abstract B09: Phosphorylation of BRAF by AMPK impairs BRAF-KSR1 association and cell proliferation." In Abstracts: AACR Special Conference on Advances in Melanoma: From Biology to Therapy; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.mel2014-b09.
Повний текст джерелаUmemura, Masanari, Erdene Baljinnyam, Mariana S. De Lorenzo, Stefan Feske, Lai-Hua Xie, and Kousaku Iwatsubo. "Abstract 1864: Role of store-operated Ca2+ entry in proliferation and cell cycle in melanoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1864.
Повний текст джерелаZHANG, YUNA YUAN, Xu Guang Yan, Margaret Farrelly, Hamed Yari, Yuchen Feng, Ting La, Hessam Tabatabaee, Lei Jin, and Xu Dong Zhang. "Abstract 2451: Long noncoding RNA OVAAL promotes melanoma cell proliferation through translational suppression of p27." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2451.
Повний текст джерелаShah, Raj, Mengying Zhu, Andrew Boreland, Fabian Filipp, and Suzie Chen. "Abstract 5493: Targeted inhibition of glutaminase in GRM1-expressing melanoma cells inhibits cell proliferation by reducing glutamate bioavailability." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5493.
Повний текст джерелаLee, Chih-Shia, Karl J. Dykema, Danielle M. Hawkins, Kyle A. Furge, and Nicholas S. Duesbery. "Abstract LB-232: MEK2 signaling pathway alone is sufficient but not necessary for melanoma cell proliferation." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-232.
Повний текст джерелаGanguly, Sourik S., Leann S. Fiore, Jonathan T. Sims, J. Woodrow Friend, DivyaMani Srinivasan, Matthew Thacker, Michael L. Cibull, Wang Chi, and Rina Plattner. "Abstract C51: c-Abl and Arg are activated in human primary melanomas, promote melanoma cell invasion, proliferation, survival, and drive metastatic progression." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-c51.
Повний текст джерела