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A20 Cell - Crossref

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Last Updated: 10 June 2022

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Abstract A20: Deacetylation of histone H3 at lysine 9 with ethanol in human colonic epithelial cells

"We therefore investigated the effect of ethanol on histone H3 changes in colonic epithelial cells. " The acetylation and methylation states of histone H3K9 were determined by immunoblot analysis using site-specific antibodies, and then the acetylation and methylation states of histone H3K9 were measured by immunoblot analysis using site-specific antibodies. We discovered that ethanol reduced acetylation of histone H3K9 in a time-dependent manner, while histone deacetylase inhibitor, trichostatin A, which was used as a positive control, raised H3K9 acetylation. ".

Source link: https://doi.org/10.1158/1940-6207.prev-08-a20


Abstract A20: Investigating the role of cell cycle proteins and CDK4/6 inhibitor PD0332991 in the redifferentiation of irreversible dysplasia

"Abstract Background: The reversal of premalignant disease by re-differentiation is an important component of cancer prevention therapy regimens. " In addition, knowing early changes during preneoplastic dysplasia can provide diagnostic and therapeutic guidance for cancer prevention campaigns. Identifying biomarkers of dysplasia reversal of dysplasia as well as mechanisms of malignant transformation from preneoplastic disease to cancer would be critical in drug design for chemoprevention strategies. Preclinical mouse models of reversible and refractory dysplasia help identify the causes of irreversible disease progression and highlight potential targets for disease reversal and prevention. In reversible and irreversible stages of epithelial dysplasia, Evaluate cell cycle regulatory network proteins. After inhibition of CDK4/6, Evaluate cell cycle protein expression changes. Previous studies showed that refractory dysplasia is a field disease with no chromosomal rearrangements. Cell cycle regulatory protein expression patterns were compared by western blot and IHC tests at the 4 and 7 month stages. PD0332991 inhibitor was given to a 7-month stage of dysplasia to check the chemopreventive role of CDK4/6 inhibition. Doxycycline was administered in the highest recommended dose of PD0339221 for ten days by gavage, according to the author. In a self-renewing cyclical fashion, the pattern of expression shows that irreversible refractory dysplasia is linked to persistent up-regulation of Cyclin D1 and CDK4/6, coupled with subsequent Rb phosphorylation and elevated levels of DP-1 and E2F in a self-renewing cyclical manner. Cell cycle proteins play a key role in dysplasia maintenance and are identified targets for cancer chemoprevention, according to the results.

Source link: https://doi.org/10.1158/1940-6207.prev-11-a20


Abstract A20: Insulin receptor signaling in mammary epithelial cells

"Insulin receptor is present in several human BCs, and the initiation of the IR/receptor kinase signaling pathway is typical of most BCs. " We hypothesize that ectopic expression of IR in BCs sensitizes BC cells to insulin action, resulting in signaling events specific to epithelial cells that are functionally different from physiological insulin-target tissues. We have used the newly developed Mammalian Membrane Two Hybrid screen to find IR interactors in human mammary epithelial MCF10A cells to help better understand the role of IR in BC. The epithelial cell IR-interactome, in turn, is intended to give an insight into RTK signaling in BC's contribution to the activation of RTK signaling and provide a roadmap for further research into IR signaling in cancer. ".

Source link: https://doi.org/10.1158/1538-8514.pi3k14-a20


Abstract A20: ARHGEF2 inhibition impairs cell growth and viability in KRAS-dependent cancer cells

"ARHGEF2 is a microtubule-associated guanine nucleotide exchange factor for the Rho family of small GTPases whose expression is up-regulated following Ras neoplastic change in Rat fibroblasts," says a researcher. ARHGEF2 has been recently identified as a transcriptional target of the RAS/MAPK pathway, and its expression has been linked to cell survival and cell proliferation in RAS-transformed cells. In several KRAS mutant cancer cell lines, we tested to see if ARHGEF2 is needed for tumour cell viability. Cell growth and viability in six different cancer cell lines harboring a KRAS mutation were monitored in six separate cancer cell lines harboring a KRAS mutation: four pancreatic adenocarcinoma, one endometrial adenocarcinoma, and one colorectal adenocarcinoma. In half of the cell lines that were tested, we found that ARHGEF2 is essential for cell growth and survival. For those cell lines, we developed an ARHGEF2 and KRAS dependency index, and further examination revealed a positive correlation between ARHGEF2 and KRAS dependency, which led to a positive correlation between ARHGEF2 and KRAS dependency. Our results show that: i/ARHGEF2 is involved in the cell lines' proliferation and survival of KRAS-dependent cell lines, but that further in vitro and in vivo studies are required; i/ARHGEF2 inhibition could be a potential therapeutic target in tumors harboring KRAS mutations. Expression cloning of lfc, a novel oncogene with structural similarities to ncleotide exchange factors and to the protein kinase C. J Biol Chem. Cell growth and viability in KRAS-dependent cancer cells is hampered by ARHGEF2 inhibition, which is an inhibitor of cell growth and survival. ".

Source link: https://doi.org/10.1158/1557-3125.rasonc14-a20


Abstract A20: Investigating the role of SCO2 in the metabolic adaptation of cancer cells

"SCO2-/- cells also have elevated intracellular oxygen and nicotinamide adenine dinucleotide levels, which results in increased reactive oxygen species and oxidative DNA damage," said the authors. With the exception of pyruvate, the steady-state values of most of the glycolytic intermediates were elevated in SCO2-/- as compared to WT cells. In turn, succinate and 2-hydroxyglutarate were higher in SCO2-/- when compared to WT cells. Also, the level of aspartate and asparagine in the SCO2-/- HCT 116 cells was found to be lower in the SCO2-/-HCT 116 cells, which is most likely to have arisen from the SCO2-/-HCT 116 cells' deficiencies in oxidative phosphorylation attributed to SCO2 loss. To track the movement of carbon atoms extracted from glucose, a stable isotope tracer analysis using 13C labeled glucose was performed. Comparing to the WT cells, SCO2-/- cells have no flux of carbon into the TCA cycle via acetyl CoA production, as expected. In SCO2-/- cells, rpS6 and 4E-BP1 were significantly less phosphorylated compared to WT, which demonstrated a halt of mTORC1 development after SCO2 loss. As shown by increased GSK3 and AKT phosphorylation, AKT and possibly mTORC2 activity in SCO2-/- cells and possibly mTORC2 activity in SCO2-/- cells as compared to WT cells. We hypothesize AMPK to maintain energy balance in the cells where mitochondrial ATP production is reduced due to the loss of complex IV function. [abstract]: "Aboutt]: "Investing the role of SCO2 in cancer cell metabolism [abstract]" is the goal of this study.

Source link: https://doi.org/10.1158/1557-3125.pi3k-mtor18-a20


Abstract A20: Excess centrosomes induce p53-dependent senescence in endothelial cells

"Therefore, knowing how excess centrosomes influence cell growth and tumor angiogenesis is crucial for studying tumor progression and tumor angiogenesis. " Cells with a lack of centrosomes undergo bipolar cell division in order to produce viable progeny, as shown by previous studies. However, we found that endothelial cells were not able to maintain the percentage of cells with excess centrosomes, meaning that excess centrosomes had no effect on endothelial cell cycle. Ser33's analysis indicates that HUVEC with excess centrosomes stimulated p53 by phosphorylating p53. Since endothelial cells maintain different cell shapes and behavior in a 3-dimensional environment relative to 2D, we investigated whether excess centrosomes cause senescence in 3D. centrosome over-duplicated ECs in 3D sprouts demonstrated SA-u03b2-gal growth, suggesting that they did not undergo senescence. We used a sprouting angiogenesis assay and found that centrosome over-duplicated ECs in 3D sprouts had SA-u03b2-gal activity, suggesting that they did not undergo senescence. Orlando, Florida; Feb 28 - Mar 2, 2016; Proceedings of the AACR Precision Medicine Series: Tumor Progression and Therapeutic Response; AACR Precision Medicine Series: Cancer Cell Cycle - Tumor Progression and Therapeutic Response; Oct 28-Mar 2, 2016.

Source link: https://doi.org/10.1158/1557-3125.cellcycle16-a20


Abstract A20: Mitochondrial phosphoenolpyruvate carboxykinase (PCK2) regulates metabolic adaptation and enables glucose-independent tumor cell growth

When nutrients are scarce, cancer cells must survive and proliferate when nutrients are lacking. " To identify metabolic pathways that promote glucose-independent tumor cell growth, we used combined transcriptional-metabolomic network analysis. In glucose deprivation, glucose deprivation aided in the rewiring of the tricarboxylic acid cycle and early steps of gluconeogenesis, which promote cell proliferation in the presence of low glucose. The development of phosphoenolpyruvate from glutamine, which was used to fuel biosynthetic pathways normally favored by glucose, such as serine and purine biosynthesis, was promoted by Glucose limitation. PCK2 expression was highly dependent on the hypoxia-inducible factors and was required to maintain tumor cell proliferation under reduced glucose availability. Many human tumor types are present, as well as enriched in tumor tissue from non-small cell lung cancer patients. "Our findings support a new role for PCK2 in cancer cell metabolic reprogramming that supports glucose-independence cell growth and metabolic stress resistance in human tumors. ".

Source link: https://doi.org/10.1158/1557-3125.metca15-a20


A20 Inhibits β-Cell Apoptosis by Multiple Mechanisms and Predicts Residual β-Cell Function in Type 1 Diabetes

"We now have evidence that A20 has broader consequences in wretched A20 and islets isolated from the u03b2-cell-specific A20 knockout mice than are not limited to inhibition of NF-u03baB. " We then discovered that the risk allele of TNFAIP3's rs2327832 single nucleotide polymorphism of T1D in a cohort of T1D children had reduced serum peptide and elevated hemoglobin A1c levels 12 months after disease onset, suggesting reduced residual u03b2-cell function and poor glycemic control. Our findings, in conclusion, show that A20 is playing a vital part in the regulation of u03b2-cell survival and inventing novel techniques by which A20 controls u03b2-cell fate. Moreover, we also identified the single nucleotide polymorphism rs2327832 of TNFAIP3 as a potential prognostic marker for diabetes risk in children with T1D.

Source link: https://doi.org/10.1210/me.2015-1176


Reduced Levels of A20 Protein Prompted RIPK1-Dependent Apoptosis of Vascular Endothelial Cells and Blood–Brain Barrier Breakdown in CIRI

"However, the specific mechanism of cell death of vascular endothelial cells is not clear. " It was discovered that ischemic reperfusion resulted in RIPK1 activation in vascular endothelial cells and in cells, which in induced cell death and subsequent RIPK1-dependent apoptosis. The purpose of this research was to investigate the role of RIPK1 in the BBB leakage during the ischemia reperfusion procedure. Embested mice or transplant mice were investigated using immunohistochemistry methods. The level of A20 protein in vascular endothelial cells was significantly reduced by proteomics, which was shown by proteomics. The involvement of RIPK1 in vascular endothelial cell death and BBB leakage after cerebral ischemia reperfusion injury has been found in this study, and these results provide a novel view on ischemic reperfusion therapy.

Source link: https://doi.org/10.21203/rs.3.rs-860675/v1


The tumor necrosis factor alpha-induced protein 3 (TNFAIP3, A20) imposes a brake on antitumor activity of CD8 T cells

"Here, mice with selective deletion of A20 in mature conventional T cells with no discernable pathology," says the author. With increased production of IL-2 and IFN, this mice's increased antigen sensitivity was demonstrated. In vivo, A20-deleted CD8 T cells exhibited elevated antitumor activity. Targeting this gene in adoptively transferred CD8 T cells could be a promising way to induce tumor rejection. ".

Source link: https://doi.org/10.1073/pnas.1406259111

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