oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
Antitumor Activity of T Cells Generated from Lymph Nodes Draining the SEA-expressing Murine B16 Melanoma and Secondarily Activated with Dendritic Cells
Jiyun Yu, Rong Tian, Bingshui Xiu, Jinqi Yan, Rui Jia, Liang Zhang, Alfred E. Chang, Hongbin Song, Qiao Li
International Journal of Biological Sciences , 2009,
Abstract: The successful use of tumor-draining lymph nodes (TDLN) as a source of effector cells for cancer immunotherapy depends largely on the immunogenicity of the tumor drained by the lymph nodes as well as the methods for secondary in vitro T cell activation and expansion. We transferred the bacterial superantigen staphylococcal enterotoxin A (SEA) gene into B16 murine melanoma tumor cells, and used them to induce TDLN (SEA TDLN) in syngeneic hosts. Wild-type (wt) TDLN induced by parental B16 tumor was used as a control. In vitro, SEA TDLN cells proliferated more vigorously, produced more IFNγ and demonstrated higher CTL activity than wt TDLN cells when activated with anti-CD3/anti-CD28/IL-2. In vivo, SEA TDLN cells mediated tumor eradication more effectively than similarly activated wt TDLN cells (p<0.01). Furthermore, use of dendritic cells (DC) plus tumor antigen in vitro in addition to anti-CD3/anti-CD28/IL-2 stimulation further amplified the immune function and therapeutic efficacy of SEA TDLN cells. DC-stimulated SEA TDLN cells eliminated nearly 90% of the pulmonary metastasis in mice bearing established B16 melanoma micrometastases. These results indicate that enforced expression of superantigen SEA in poorly immunogenic tumor cells can enhance their immunogenicity as a vaccine in vivo. The combined use of genetically modified tumor cells as vaccine to induce TDLN followed by secondary stimulation using antigen-presenting cells and tumor antigen in a sequential immunization/activation procedure may represent a unique method to generate more potent effector T cells for adoptive immunotherapy of cancer.
In Vitro and in Vivo Anticancer Activity of Aconitine on Melanoma Cell Line B16  [PDF]
Juan Du,Xiaonian Lu,Ziwen Long,Zhen Zhang,Xiaohua Zhu,Yongsheng Yang,Jinhua Xu
Molecules , 2013, DOI: 10.3390/molecules18010757
Abstract: The anti-tumor effect of aconitine in melanoma cell line B16 has been studied in this paper. We found that B16 cells showed significantly reduced growth rates and increased apoptotic effects in the presence of aconitine. Furthermore, aconitine inhibited the PI3K/AKT and MAPK/ERK1/2 signaling pathways, thus regulating the levels of protein and mRNA of PCNA and apoptotic related signaling molecules. Above all, we found that aconitine showed an anti-melanoma effect in suppressing tumor growth in vivo. In conclusion, we show that aconitine may be a useful anticancer drug in the future.
Enhanced antitumor effects of tumor antigen-pulsed dendritic cells by their transfection with GM-CSF gene
Xuetao Cao,Weiping Zhang,Shihua Ma,Minghui Zhang,Jianli Wang,Tianxing Ye
Science China Life Sciences , 1997, DOI: 10.1007/BF03183594
Abstract: To investigate the biological characterization and antitumor activities of GM-CSF gene-transfected dendritic cells, the splenic dendritic cells were infected with GM-CSF recombinant replication-deficient adenovirusesin vitro. Their enhanced expression of B7 was demonstrated by FACS analysis, and more potent stimulatory activity was confirmed by allogeneic MLR. Immunization of dendritic cells pulsed with irradiated B16 melanoma cells induced significant CTL and enabled host to resist the challenge of wild-type B16 cells. When they were transfected with GM-CSF gene subsequently, the induced CTL activity was higher, and the produced protection against B16 cell challenge and therapeutic effect on the mice with preestablished pulmonary metastases more effective. These data suggest that the dendritic cells pulsed with tumor antigen then transfected with GM-CSF gene can be used as an effective vaccine in tumor immunotherapy.
Acute and Long-Term Effects of Hyperthermia in B16-F10 Melanoma Cells  [PDF]
Mónica Pereira Garcia, José Roberto Tinoco Cavalheiro, Maria Helena Fernandes
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035489
Abstract: Objective Hyperthermia uses exogenous heat induction as a cancer therapy. This work addresses the acute and long-term effects of hyperthermia in the highly metastatic melanoma cell line B16-F10. Materials and Methods Melanoma cells were submitted to one heat treatment, 45°C for 30 min, and thereafter were kept at 37°C for an additional period of 14 days. Cultures maintained at 37°C were used as control. Cultures were assessed for the heat shock reaction. Results Immediately after the heat shock, cells began a process of fast degradation, and, in the first 24 h, cultures showed decreased viability, alterations in cell morphology and F-actin cytoskeleton organization, significant reduction in the number of adherent cells, most of them in a process of late apoptosis, and an altered gene expression profile. A follow-up of two weeks after heat exposure showed that viability and number of adherent cells remained very low, with a high percentage of early apoptotic cells. Still, heat-treated cultures maintained a low but relatively constant population of cells in S and G2/M phases for a long period after heat exposure, evidencing the presence of metabolically active cells. Conclusion The melanoma cell line B16-F10 is susceptible to one hyperthermia treatment at 45°C, with significant induced acute and long-term effects. However, a low but apparently stable percentage of metabolically active cells survived long after heat exposure.
Enhanced antitumor effects of tumor antigen-pulsed dendritic cells by their transfection with GM-CSF gene
CAO Xuetao,ZHANG Weiping,MA Shihua,ZHANG Minghui,WANG Jianli,YE Tianxing,
曹雪涛
,章卫平,马施华,张明徽,王建莉,叶天星

中国科学C辑(英文版) , 1997,
Abstract: To investigate the biological characterization and antitumor activitites of GM-CSF gene-transfected dendritic cells, the splenic dendritic cells were infected with GM-CSF recombinant replication-deficient adenoviruses in vitro . Their enhanced expression of B7 was demonstrated by FACS analysis, and more potent stimulatory activity was confirmed by allogeneic MLR. Immunization of dendritic cells pulsed with irradiated B16 melanoma cells induced sig-nificant CTL and enabled host to resist the challenge of wild-type B16 cells. When they were transfected with GM-CSF gene subsequently, the induced CTL activity was higher, and the produced protection against B16 cell challenge and therapeutic effect on the mice with preestablished pulmonary melastases more effective. These data suggest that the dendritic cells pulsed with tumor antigen then transfected with GM-CSF gene can be used as an effective vaccine in tumor immunotherapy.
Glucocorticoid Receptor Knockdown Decreases the Antioxidant Protection of B16 Melanoma Cells: An Endocrine System-Related Mechanism that Compromises Metastatic Cell Resistance to Vascular Endothelium-Induced Tumor Cytotoxicity  [PDF]
Elena Obrador, Soraya L. Valles, María Benlloch, J. Antoni Sirerol, José A. Pellicer, Javier Alcácer, Javier Alcácer-F. Coronado, José M. Estrela
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0096466
Abstract: We previously reported an interorgan system in which stress-related hormones (corticosterone and noradrenaline), interleukin-6, and glutathione (GSH) coordinately regulate metastatic growth of highly aggressive B16-F10 melanoma cells. Corticosterone, at levels measured in tumor-bearing mice, also induces apoptotic cell death in metastatic cells with low GSH content. In the present study we explored the potential role of glucocorticoids in the regulation of metastatic cell death/survival during the early stages of organ invasion. Glucocorticoid receptor (GCR) knockdown decreased the expression and activity of γ-glutamylcysteine synthetase (γ-GCS), the rate-limiting step in GSH synthesis, in metastatic cells in vivo independent of the tumor location (liver, lung, or subcutaneous). The decrease in γ-GCS activity was associated with lower intracellular GSH levels. Nrf2- and p53-dependent down-regulation of γ-GCS was associated with a decrease in the activities of superoxide dismutase 1 and 2, catalase, glutathione peroxidase, and glutathione reductase, but not of the O2?-generating NADPH oxidase. The GCR knockdown-induced decrease in antioxidant protection caused a drastic decrease in the survival of metastatic cells during their interaction with endothelial cells, both in vitro and in vivo; only 10% of cancer cells attached to the endothelium survived compared to 90% survival observed in the controls. This very low rate of metastatic cell survival was partially increased (up to 52%) in vivo by inoculating B16-F10 cells preloaded with GSH ester, which enters the cell and delivers free GSH. Taken together, our results indicate that glucocorticoid signaling influences the survival of metastatic cells during their interaction with the vascular endothelium.
Three-Dimensional Analysis of Melanosomes Isolated from B16 Melanoma Cells by Using Ultra High Voltage Electron Microscopy  [PDF]
Shuuichi Akazaki, Toshie Takahashi, Yujiro Nakano, Tomoki Nishida, Hirotarou Mori, Akio Takaoka, Hitomi Aoki, Huayua Chen, Takahiro Kunisada, Kenzo Koike
Microscopy Research (MR) , 2014, DOI: 10.4236/mr.2014.21001
Abstract:

Melanosomes, isolated by centrifugal separation from culture broth of B16 melanoma cells derived from mouse, were observed by scanning electron microscopy (SEM), and by transmission electron microscopy (TEM). Some interesting structural features were found inside and outside of the melanosomes. By SEM observation, the melanosomes were ellipsoid shape, their surface was not smooth and was covered with rough substructure, 10 to 20 nm particles. By TEM, uneven structure and micro particles were observed in the melanosomes. Furthermore, three-dimensional analysis was tried by using the ultra-high voltage electron microscopy(UHVEM). Micrographs of the melanosomes were taken at various tilted angles by UHVEM, after preparing 500 nm thickness specimens stained with lead citrate. From the micrographs collected, the three-dimensional structures were reconstructed by using i-mode software. Melanin stained by lead and non stained parts was clearly observed in the reconstructed structure. Non stained parts were round, regular size, and distributed widely in the melanosomes.

Paullinia cupana Mart var. sorbilis, guaraná, reduces cell proliferation and increases apoptosis of B16/F10 melanoma lung metastases in mice
Fukumasu, H.;Avanzo, J.L.;Nagamine, M.K.;Barbuto, J.A.;Rao, K.V.;Dagli, M.L.Z.;
Brazilian Journal of Medical and Biological Research , 2008, DOI: 10.1590/S0100-879X2008000400008
Abstract: we showed that guaraná (paullinia cupana mart var. sorbilis) had a chemopreventive effect on mouse hepatocarcinogenesis and reduced diethylnitrosamine-induced dna damage. in the present experiment, we evaluated the effects of guaraná in an experimental metastasis model. cultured b16/f10 melanoma cells (5 x 105 cells/animal) were injected into the tail vein of mice on the 7th day of guaraná treatment (2.0 mg p. cupana/g body weight, per gavage) and the animals were treated with guaraná daily up to 14 days until euthanasia (total treatment time: 21 days). lung sections were obtained for morphometric analysis, apoptotic bodies were counted to calculate the apoptotic index and proliferating cell nuclear antigen-positive cells were counted to determine the proliferation index. guaraná-treated (gua) animals presented a 68.6% reduction in tumor burden area compared to control (co) animals which were not treated with guaraná (co: 0.84 ± 0.26, n = 6; gua: 0.27 ± 0.24, n = 6; p = 0.0043), a 57.9% reduction in tumor proliferation index (co: 23.75 ± 20.54, n = 6; gua: 9.99 ± 3.93, n = 6; p = 0.026) and a 4.85-fold increase in apoptotic index (co: 66.95 ± 22.95, n = 6; gua: 324.37 ± 266.74 ab/mm2, n = 6; p = 0.0152). in this mouse model, guaraná treatment decreased proliferation and increased apoptosis of tumor cells, consequently reducing the tumor burden area. we are currently investigating the molecular pathways of the effects of guaraná in cultured melanoma cells, regarding principally the cell cycle inhibitors and cyclins.
新基因AY358935对B16细胞小鼠体内外生长的影响
Effect of a new gene AY358935 on growth of mouse melanoma B16 cells in vivo and in vitro
 [PDF]

熊绍权,,,李亚玲,王莉娟,罗秋月,宋婷婷,,,李世杰,何成诗
- , 2018, DOI: 10.13705/j.issn.1671-6825.2017.11.078
Abstract: 目的:探讨新基因AY358935对小鼠黑色素瘤B16在细胞小鼠体内外生长的影响及其可能的机制。方法:构建小鼠AY358935基因真核表达质粒并稳定转染B16细胞。MTT法检测AY358935转染细胞(B16-mAY细胞)、空质粒pcDNA3.1转染细胞(B16-pcDNA3.1细胞)及未转染的B16细胞的体外增殖活性。将B16-mAY及B16-pcDNA3.1细胞分别腹背皮下接种于C57小鼠,观察两组成瘤情况。MTT法检测B16-mAY细胞培养上清对人脐静脉内皮细胞(HUVEC)增殖的影响。结果:B16-mAY细胞的体外增殖活性明显高于B16-pcDNA3.1细胞及对照B16细胞(P<0.05)。B16-mAY细胞移植瘤体积较B16-pcDNA3.1组明显增大(P<0.05)。B16-mAY细胞培养上清组HUVEC增殖活性明显高于B16-pcDNA3.1培养上清组(P<0.05)。结论:AY358935具有促进B16细胞生长的作用,其机制可能涉及促血管生长。
Aim: To explore the effect of a new gene AY358935 on the growth of mouse melanoma B16 cells and its possible mechanism.Methods: The eukaryotic expression plasmid of AY358935 was created and stably transfected to the B16 cells. The growth of the B16 cells transfected with the AY358935(B16-mAY cells), with the pcDNA3.1 plasmid(B16-pcDNA3.1 cells)and the untransfected B16 cells was detected by MTT method.The B16-mAY cells and the B16-pcDNA3.1 cells were inoculated to the C57 mice through the way of back-belly subcutaneous inoculation, and the tumor volume were detected.The effect of the B16-mAY cells cultured supernatant on the growth of human umbilical vein endothelial cells(HUVEC)were detected by MTT method.Results: The proliferation activity of B16-mAY cells in vitro were significantly faster than those of B16-pcDNA3.1 cells and B16 cells(P<0.05). The tumor volume of the mice inoculated with B16-mAY cells were significantly bigger than that of B16-pcDNA3.1 cells group(P<0.05). The proliferation activity of HUVEC cultivated in cultured supernatant of B16-mAY cells was significantly higher than B16-pcDNA3.1 cells(P<0.05).Conclusion: AY358935 can promote the growth of B16 cells, and the mechanism may be involved in promoting the growth of blood vessel
Direct Contact with Endoderm-Like Cells Efficiently Induces Cardiac Progenitors from Mouse and Human Pluripotent Stem Cells  [PDF]
Hideki Uosaki, Peter Andersen, Lincoln T. Shenje, Laviel Fernandez, Sofie Lindgren Christiansen, Chulan Kwon
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0046413
Abstract: Rationale Pluripotent stem cell–derived cardiac progenitor cells (CPCs) have emerged as a powerful tool to study cardiogenesis in vitro and a potential cell source for cardiac regenerative medicine. However, available methods to induce CPCs are not efficient or require high-cost cytokines with extensive optimization due to cell line variations. Objective Based on our in-vivo observation that early endodermal cells maintain contact with nascent pre-cardiac mesoderm, we hypothesized that direct physical contact with endoderm promotes induction of CPCs from pluripotent cells. Method and Result To test the hypothesis, we cocultured mouse embryonic stem (ES) cells with the endodermal cell line End2 by co-aggregation or End2-conditioned medium. Co-aggregation resulted in strong induction of Flk1+ PDGFRa+ CPCs in a dose-dependent manner, but the conditioned medium did not, indicating that direct contact is necessary for this process. To determine if direct contact with End2 cells also promotes the induction of committed cardiac progenitors, we utilized several mouse ES and induced pluripotent (iPS) cell lines expressing fluorescent proteins under regulation of the CPC lineage markers Nkx2.5 or Isl1. In agreement with earlier data, co-aggregation with End2 cells potently induces both Nkx2.5+ and Isl1+ CPCs, leading to a sheet of beating cardiomyocytes. Furthermore, co-aggregation with End2 cells greatly promotes the induction of KDR+ PDGFRa+ CPCs from human ES cells. Conclusions Our co-aggregation method provides an efficient, simple and cost-effective way to induce CPCs from mouse and human pluripotent cells.
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.