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Calcium Electroporation – A Novel Treatment to Overcome Cancer-Mediated Immune Suppression
Published in Marko S. Markov, James T. Ryaby, Erik I. Waldorff, Pulsed Electromagnetic Fields for Clinical Applications, 2020
Adenosine, a by-product of ATP catabolism, is the ligand for the A2AR and is known for having immune-stimulating and immune-suppressing activity. When ATP is released from damaged cells, it acts as a potent inductor of various immune cells including dendritic cells, NK cells, and T-cells through its binding action to P2X receptors (Sachet, Liang, & Oehler, 2017). On the other hand, when ATP is degraded to adenosine through ectoenzymes CD39 and CD73, it is known to suppress T-cell activation via the A2AR (Ohta, 2016).
Role of Histone Methyltransferase in Breast Cancer
Published in Meenu Gupta, Rachna Jain, Arun Solanki, Fadi Al-Turjman, Cancer Prediction for Industrial IoT 4.0: A Machine Learning Perspective, 2021
Surekha Manhas, Zaved Ahmed Khan
TGF-β makes it critical to express CD103 and IL-17A/F in Treg and Th17 cells by downregulation, the expression of GFI1 up to that extent [81]. Furthermore, it also inhibits CD73 and CD39 ectonucleotidase expressions [82]. For the activation reduction of methylation marks, lysine demethylae LSD1 recruitment is carried out by GFI1 to the mentioned genetic loci. Upon TGF-β stimulation, gene expression of GFI1 gets reduced, which allows the cellular differentiation of Treg and Th17 cells optimally. T cells that lack GFI1 display an increase in IL-17A production and an increase in the expression of FOXP3 in response to transforming growth factor-beta (TGF-β) that shows similarities with G9a-deficient lymphocytes, specifically T cells [14]. As dysregulated IL-17A expression was observed in Th2 cells with a lack of G9a, the same was observed with GFI1, which is basically required to silence the expression of IL-17A found in lymphocytes [15,81]. Consequently, it is very interesting to specifically hypothesize about interactions between GFI1–G9a. Specifically, they are more critical in restraining the cellular-based responses of Treg cells along with Th17 cells, resulting in repression in the transcriptional mechanism that leads to epigenetic gene inactivation or gene silencing. For the type 11 innate lymphoid cell (ILC2) development and cellular functions, GFI1 usually acts as an important potent regulator [83]. GFI1 expression is correlated to the ST2-based receptor IL-33 expression (Il1rl1, ST2), along with the expression of GATA3. GFI1 loss in ILC2s results in the impairment of GATA3 expressions and IL-17A expression upregulation, too. It is reminiscent of the specified G9a role in ILC biology, where G9a is needed to repress the actions of genes specifically related to ILC during the development of ILC2 [69], although, unlike T cells, the GFI1 effect and potentially G9a seem to be reliant on methyltransferase-dependent repressive activity of the specific gene. By analyzing all the available dates, which suggest G9a–GFI1 are critical to performing functions in ILCs and T cells, future studies defining these interactions on the basis of molecular level might open new ways for novel therapeutics that might inhibit the dysregulated responses of Th2 cell-related to other diseases like allergies and asthma.
Insights of ethyl acetate fraction from Vassobia breviflora in multidrug-resistant bacteria and cancer cells: from biological to therapeutic
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Altevir Rossato Viana, Nathieli Bianchin Bottari, Daniel Santos, Marissa Bolson Serafin, Bruna Garlet Rossato, Rafael Noal Moresco, Katianne Wolf, Aline Ourique, Rosmari Hörner, Érico Marlon de Moraes Flores, Maria Rosa Chitolina Schetinger, Bruno Stefanello Vizzotto, Luciana Maria Fontanari Krause
In this study V. breviflora increased NTPDase activity when ATP was used as a substrate. It became evident that during cell apoptosis, high levels of extracellular ATP are released. The enzymatic activity of CD39 and CD73 is, therefore, able to modulate the duration and magnitude of purinergic signaling through the ATP-CD39-CD73-Ado cascade, as CD39 hydrolyzes extracellular ATP to AMP and CD73 dephosphorylates AMP to Ado, a critical regulator in both innate immune systems response mechanisms and adaptive immune response, where CD39 acts as a limiting enzyme for this cascade. The lower expression of these ectonucleotidases involved in the catabolism of ADP and AMP is considered a signal of nucleoside and nucleoside modulation.