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1.
Fernanda Fai?o-Flores Paulo Rogério Pinto Coelho Jo?o Dias Toledo Arruda-Neto Silvya Stuchi Maria-Engler Manoela Tiago Vera Luiza Capelozzi Ricardo Rodrigues Giorgi Durvanei Augusto Maria 《PloS one》2013,8(3)
Boron neutron capture therapy (BNCT) is a binary treatment involving selective accumulation of boron carriers in a tumor followed by irradiation with a thermal or epithermal neutron beam. The neutron capture reaction with a boron-10 nucleus yields high linear energy transfer (LET) particles, alpha and 7Li, with a range of 5 to 9 µm. These particles can only travel very short distances and release their damaging energy directly into the cells containing the boron compound. We aimed to evaluate proliferation, apoptosis and extracellular matrix (ECM) modifications of B16F10 melanoma and normal human melanocytes after BNCT. The amounts of soluble collagen and Hsp47, indicating collagen synthesis in the ECM, as well as the cellular markers of apoptosis, were investigated. BNCT decreased proliferation, altered the ECM by decreasing collagen synthesis and induced apoptosis by regulating Bcl-2/Bax in melanoma. Additionally, BNCT also increased the levels of TNF receptor and the cleaved caspases 3, 7, 8 and 9 in melanoma. These results suggest that multiple pathways related to cell death and cell cycle arrest are involved in the treatment of melanoma by BNCT. 相似文献
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Krishna SS Tautz L Xu Q McMullan D Miller MD Abdubek P Ambing E Astakhova T Axelrod HL Carlton D Chiu HJ Clayton T DiDonato M Duan L Elsliger MA Grzechnik SK Hale J Hampton E Han GW Haugen J Jaroszewski L Jin KK Klock HE Knuth MW Koesema E Morse AT Mustelin T Nigoghossian E Oommachen S Reyes R Rife CL van den Bedem H Weekes D White A Hodgson KO Wooley J Deacon AM Godzik A Lesley SA Wilson IA 《Proteins》2007,69(2):415-421
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Mathews II Krishna SS Schwarzenbacher R McMullan D Jaroszewski L Miller MD Abdubek P Agarwalla S Ambing E Axelrod HL Canaves JM Carlton D Chiu HJ Clayton T DiDonato M Duan L Elsliger MA Grzechnik SK Hale J Hampton E Haugen J Jin KK Klock HE Koesema E Kovarik JS Kreusch A Kuhn P Levin I Morse AT Nigoghossian E Okach L Oommachen S Paulsen J Quijano K Reyes R Rife CL Spraggon G Stevens RC van den Bedem H White A Wolf G Xu Q Hodgson KO Wooley J Deacon AM Godzik A Lesley SA Wilson IA 《Proteins》2006,65(1):249-254
4.
Han GW Sri Krishna S Schwarzenbacher R McMullan D Ginalski K Elsliger MA Brittain SM Abdubek P Agarwalla S Ambing E Astakhova T Axelrod H Canaves JM Chiu HJ DiDonato M Grzechnik SK Hale J Hampton E Haugen J Jaroszewski L Jin KK Klock HE Knuth MW Koesema E Kreusch A Kuhn P Miller MD Morse AT Moy K Nigoghossian E Oommachen S Ouyang J Paulsen J Quijano K Reyes R Rife C Spraggon G Stevens RC van den Bedem H Velasquez J Wang X West B White A Wolf G Xu Q Hodgson KO Wooley J Deacon AM Godzik A 《Proteins》2006,64(4):1083-1090
5.
Xu Q Krishna SS McMullan D Schwarzenbacher R Miller MD Abdubek P Agarwalla S Ambing E Astakhova T Axelrod HL Canaves JM Carlton D Chiu HJ Clayton T DiDonato M Duan L Elsliger MA Feuerhelm J Grzechnik SK Hale J Hampton E Han GW Haugen J Jaroszewski L Jin KK Klock HE Knuth MW Koesema E Kreusch A Kuhn P Morse AT Nigoghossian E Okach L Oommachen S Paulsen J Quijano K Reyes R Rife CL Spraggon G Stevens RC van den Bedem H White A Wolf G Hodgson KO Wooley J Deacon AM Godzik A Lesley SA Wilson IA 《Proteins》2006,65(3):777-782
6.
DiDonato M Krishna SS Schwarzenbacher R McMullan D Agarwalla S Brittain SM Miller MD Abdubek P Ambing E Axelrod HL Canaves JM Chiu HJ Deacon AM Duan L Elsliger MA Godzik A Grzechnik SK Hale J Hampton E Haugen J Jaroszewski L Jin KK Klock HE Knuth MW Koesema E Kreusch A Kuhn P Lesley SA Levin I Morse AT Nigoghossian E Okach L Oommachen S Paulsen J Quijano K Reyes R Rife CL Spraggon G Stevens RC van den Bedem H White A Wolf G Xu Q Hodgson KO Wooley J Wilson IA 《Proteins》2006,65(3):771-776
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Sousa JF Torrieri R Silva RR Pereira CG Valente V Torrieri E Peronni KC Martins W Muto N Francisco G Brohem CA Carlotti CG Maria-Engler SS Chammas R Espreafico EM 《PloS one》2010,5(10):e13510
Melanoma is a highly aggressive and therapy resistant tumor for which the identification of specific markers and therapeutic targets is highly desirable. We describe here the development and use of a bioinformatic pipeline tool, made publicly available under the name of EST2TSE, for the in silico detection of candidate genes with tissue-specific expression. Using this tool we mined the human EST (Expressed Sequence Tag) database for sequences derived exclusively from melanoma. We found 29 UniGene clusters of multiple ESTs with the potential to predict novel genes with melanoma-specific expression. Using a diverse panel of human tissues and cell lines, we validated the expression of a subset of three previously uncharacterized genes (clusters Hs.295012, Hs.518391, and Hs.559350) to be highly restricted to melanoma/melanocytes and named them RMEL1, 2 and 3, respectively. Expression analysis in nevi, primary melanomas, and metastatic melanomas revealed RMEL1 as a novel melanocytic lineage-specific gene up-regulated during melanoma development. RMEL2 expression was restricted to melanoma tissues and glioblastoma. RMEL3 showed strong up-regulation in nevi and was lost in metastatic tumors. Interestingly, we found correlations of RMEL2 and RMEL3 expression with improved patient outcome, suggesting tumor and/or metastasis suppressor functions for these genes. The three genes are composed of multiple exons and map to 2q12.2, 1q25.3, and 5q11.2, respectively. They are well conserved throughout primates, but not other genomes, and were predicted as having no coding potential, although primate-conserved and human-specific short ORFs could be found. Hairpin RNA secondary structures were also predicted. Concluding, this work offers new melanoma-specific genes for future validation as prognostic markers or as targets for the development of therapeutic strategies to treat melanoma. 相似文献
9.
Jin KK Krishna SS Schwarzenbacher R McMullan D Abdubek P Agarwalla S Ambing E Axelrod H Canaves JM Chiu HJ Deacon AM DiDonato M Elsliger MA Feuerhelm J Godzik A Grittini C Grzechnik SK Hale J Hampton E Haugen J Hornsby M Jaroszewski L Klock HE Knuth MW Koesema E Kreusch A Kuhn P Lesley SA Miller MD Moy K Nigoghossian E Okach L Oommachen S Paulsen J Quijano K Reyes R Rife C Stevens RC Spraggon G van den Bedem H Velasquez J White A Wolf G Han GW Xu Q Hodgson KO Wooley J Wilson IA 《Proteins》2006,63(4):1112-1118
10.
damo Davi Digenes Siena Isabela Ichihara de Barros Camila Baldin Storti Carlos Alberto Oliveira de Biagi Júnior Larissa Anastacio da Costa Carvalho Silvya Stuchi MariaEngler Josane de Freitas Sousa Wilson Araújo Silva Jr 《Journal of cellular and molecular medicine》2022,26(3):671
Our previous work using a melanoma progression model composed of melanocytic cells (melanocytes, primary and metastatic melanoma samples) demonstrated various deregulated genes, including a few known lncRNAs. Further analysis was conducted to discover novel lncRNAs associated with melanoma, and candidates were prioritized for their potential association with invasiveness or other metastasis‐related processes. In this sense, we found the intergenic lncRNA (ENSG00000230454) and decided to explore its effects in melanoma. For that, we silenced the lncRNA U73166 expression using shRNAs in a melanoma cell line. Next, we experimentally investigated its functions and found that migration and invasion had significantly decreased in knockdown cells, indicating an essential association of lncRNA U73166 for cancer processes. Additionally, using naïve and vemurafenib‐resistant cell lines and data from a patient before and after resistance, we found that vemurafenib‐resistant samples had a higher expression of lncRNA U73166. Also, we retrieved data from the literature that indicates lncRNA U73166 may act as a mediator of RNA processing and cell invasion, probably inducing a more aggressive phenotype. Therefore, our results suggest a relevant role of lncRNA U73166 in metastasis development. We also pointed herein the lncRNA U73166 as a new possible biomarker or target to help overcome clinical vemurafenib resistance. U73166相似文献