Poliglusam Nanoparticles Activate T Cell Response in Breast Cancer Cell: an In Vivo and In Vitro Study

2019 ◽  
Vol 29 (4) ◽  
pp. 1057-1064 ◽  
Author(s):  
Neda Soleimani ◽  
Akbar Vaseghi ◽  
Valentina Loconte
1998 ◽  
Vol 65 (Supplement) ◽  
pp. 199
Author(s):  
C. Baron ◽  
S. Zaiei ◽  
V. Schiavon ◽  
D. Chopin ◽  
P. Lang

2013 ◽  
Vol 8 (1) ◽  
Author(s):  
Tim Lautenschlaeger ◽  
James Perry ◽  
David Peereboom ◽  
Bin Li ◽  
Ahmed Ibrahim ◽  
...  

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Maral Mazloumi Tabrizi ◽  
Pouria Mohammadi ◽  
Afrooz Ahmadi ◽  
Mohammadreza Malekpour ◽  
Nahid Kabiry ◽  
...  

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Zhongwei Li ◽  
Diandian Wang ◽  
Xintian Chen ◽  
Wenwen Wang ◽  
Pengfei Wang ◽  
...  

AbstractProtein arginine methyltransferase 1 (PRMT1) is able to promote breast cancer cell proliferation. However, the detailed mechanisms of PRMT1-mediated breast cancer cell proliferation are largely unknown. In this study, we reveal that PRMT1-mediated methylation of EZH2 at the R342 site (meR342-EZH2) has a great effect on PRMT1-induced cell proliferation. We also demonstrate that meR342-EZH2 can accelerate breast cancer cell proliferation in vitro and in vivo. Further, we show that meR342-EZH2 promotes cell cycle progression by repressing P16 and P21 transcription expression. In terms of mechanism, we illustrate that meR342-EZH2 facilitates EZH2 binding with SUZ12 and PRC2 assembly by preventing AMPKα1-mediated phosphorylation of pT311-EZH2, which results in suppression of P16 and P21 transcription by enhancing EZH2 expression and H3K27me3 enrichment at P16 and P21 promoters. Finally, we validate that the expression of PRMT1 and meR342-EZH2 is negatively correlated with pT311-EZH2 expression. Our findings suggest that meR342-EZH2 may become a novel therapeutic target for the treatment of breast cancer.


2020 ◽  
Author(s):  
Melisa Gorosito Serrán ◽  
Facundo Fiocca Vernengo ◽  
Laura Almada ◽  
Cristian G Beccaria ◽  
Pablo F Canete ◽  
...  

ABSTRACTDuring infections with protozoan parasites or virus, T cell immunosuppression is generated simultaneously with a high B cell activation. Here, we show that in T. cruzi infection, all plasmablasts detected had higher surface expression of PD-L1, than other mononuclear cells. PD-L1hi plasmablasts were induced in vivo in an antigen-specific manner and required help from Bcl-6+CD4+T cells. PD-L1hi expression was not a characteristic of all antibody-secreting cells since plasma cells found during the chronic phase of infection express PD-L1 but at lower levels. PD-L1hi plasmablasts were also present in mice infected with Plasmodium or with lymphocytic choriomeningitis virus, but not in mice with autoimmune disorders or immunized with T cell-dependent antigens. PD-L1hi plasmablasts suppressed T cell response, via PD-L1, in vitro and in vivo. Thus, this study reveals that extrafollicular PD-L1hi plasmablasts, which precede the germinal center (CG) response, are a suppressive population in infections that may influence T cell response.Brief summaryPathogens develop different strategies to settle in the host. We identified a plasmablats population induced by pathogens in acute infections which suppress T cell response.


2014 ◽  
Vol 8 (Suppl 4) ◽  
pp. P22
Author(s):  
Klesia Madeira ◽  
Murilo Cerri ◽  
Renata Daltoé ◽  
Alice Herlinger ◽  
João Filho ◽  
...  

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