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The antimalarial drug mefloquine enhances TP53 premature termination codon readthrough by aminoglycoside G418.

Nonsense mutations constitute ~10% of TP53 mutations in cancer. They introduce a premature termination codon that gives rise to truncated p53 protein with impaired function. The aminoglycoside G418 can induce TP53 premature termination codon readthrough and thus increase cellular levels of full-length protein. Small molecule phthalimide derivatives that can enhance the readthrough activity of G418 have also been described. To determine whether readthrough enhancers exist among drugs that are already approved for use in humans, we tested seven antimalarial drugs for readthrough of the common R213X TP53 nonsense mutation in HDQ-P1 breast cancer cells. Mefloquine induced no TP53 readthrough activity as a single agent but it strongly potentiated readthrough by G418. The two enantiomers composing pharmaceutical mefloquine potentiated readthrough to similar levels in HDQ-P1 cells and also in SW900, NCI-H1688 and HCC1937 cancer cells with different TP53 nonsense mutations. Exposure to G418 and mefloquine increased p53 phosphorylation at Ser15 and P21 transcript levels following DNA damage, indicating p53 produced via readthrough was functional. Mefloquine does not appear to enhance readthrough via lysosomotropic effects as it did not significantly affect lysosomal pH, the cellular levels of G418 or its distribution in organellar or cytosolic fractions. The availability of a readthrough enhancer that is already approved for use in humans should facilitate study of the therapeutic potential of TP53 readthrough in preclinical cancer models.

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miR-885-5p plays an accomplice role in liver cancer by instigating TIGAR expression via targeting its promoter.

TIGAR (TP53-induced glycolysis and apoptosis regulator) is a p53-inducible gene, and its expression resulted in controlling metabolism and protection from apoptosis. Furthermore, TIGAR participated in promoting the pentose phosphate pathway and helping to lower intracellular reactive oxygen species (ROS). miR-885-5p has also been reported to be involved in liver tumorigenesis, but whether miR-885-5p has a regulatory effect on TIGAR expression is unknown. In this study, we found that their levels were correlated to each other and positively related to cell malignancy. Exogenous miR-885-5p induced TIGAR expression through a p53-independent pathway. The promoter region of TIGAR harbors two tandem putative miR-885-5p target sites. Cotransfection of synthetic miR-885 with TIGAR promoter reporter constructs significantly enhanced TIGAR promoter activity via binding with target sites. Furthermore, miR-885-5p and its precursor pre-miR-885 had the same stimulatory impact on TIGAR expression. ChIP analysis further verified that increased miR-885-5p potentiated the accessibility of TIGAR promoter chromatin to transcriptional factors and facilitated TIGAR expression. miR-885-5p and its precursor both can interact mechanically with TIGAR promoter binding site and alter local chromatin structure, and subsequently upregulate TIGAR expression and participate in liver tumorigenesis. This article is protected by copyright. All rights reserved.

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Bradykinin protects cardiac c-kit positive cells from high-glucose-induced senescence through B2 receptor signaling pathway.

Cardiac c-kit positive cells are cardiac-derived cells that exist within the heart and have a great many protective effects. The senescence of cardiac c-kit positive cells probably leads to cell dysfunction. Bradykinin plays a key role in cell protection. However, whether bradykinin prevents cardiac c-kit positive cells from high-glucose-induced senescence is unknown. Here, we found that glucose treatment causes the premature senescence of cardiac c-kit positive cells. Bradykinin B2 receptor (B2R) expression was declined by glucose-induced senescence. Bradykinin treatment inhibited senescence and reduced intracellular oxygen radicals according to senescence-associated β-galactosidase staining and 2',7'-dichlorodihydrofluorescein diacetate staining. Moreover, the mitochondrial membrane potential was damaged, as measured by JC-1 staining. The mitochondrial membrane potential was preserved under bradykinin treatment. The concentration of superoxide was decreased, and the concentration of intracellular adenosine triphosphate was increased after bradykinin treatment. Western blot showed that bradykinin leads to AKT and mammalian target of rapamycin (mTOR) phosphorylation and decreased levels of P53 and P16 when compared with glucose treatment alone. Antagonists of B2R, phosphoinositide 3-kinase (PI3K), mTOR, and B2R small interfering RNA prevented the protective effect of bradykinin. P53 antagonist also inhibited the glucose-induced senescence of cardiac c-kit positive cells. In conclusion, bradykinin prevents the glucose-induced premature senescence of cardiac c-kit positive cells through the B2R/PI3K/AKT/mTOR/P53 signal pathways.

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Identification of Potential Biomarkers in Glioblastoma through Bioinformatic Analysis and Evaluating Their Prognostic Value.

Glioblastoma is a common malignant tumor in the central nervous system with an extremely poor outcome; understanding the mechanisms of glioblastoma at the molecular level is essential for clinical treatment. In the present study, we used bioinformatics analysis to identify potential biomarkers associated with prognosis in glioblastoma and elucidate the underlying mechanisms. The result revealed that 552 common genes were differentially expressed between glioblastoma and normal tissues based on TCGA, GSE4290, and GSE 50161 datasets. Gene Oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and protein-protein interaction (PPI) network were carried out to gain insight into the actions of differentially expressed genes (DEGs). As a result, 20 genes (CALB1, CDC20, CDCA8, CDK1, CEP55, DLGAP5, KIF20A, KIF4A, NDC80, PBK, RRM2, SYN1, SYP, SYT1, TPX2, TTK, VEGFA, BDNF, GNG3, and TOP2A) were found as hub genes via CytoHubba in Cytoscape and functioned mainly by participating in cell cycle and p53 signaling pathway; among them, RRM2 and CEP55 were considered to have relationship with the prognosis of glioblastoma, especially RRM2. High expression of RRM2 was consistent with shorter overall survival time. In conclusion, our study displayed the bioinformatic analysis methods in screening potential oncogenes in glioblastoma and underlying mechanisms. What is more is that we successfully identified RRM2 as a novel biomarker linked with prognosis, which might be expected to be a promising target for the therapy of glioblastoma.

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Clinicopathologic and molecular characteristics of 44 patients with pure secretory breast carcinoma.

Secretory breast carcinoma (SBC) is a rare type of breast malignancy, accounting for less than 0.02% of all infiltrating breast malignancies. The pure SBC, a type of SBC without another type of breast malignant neoplasm, is particularly rare. This study aimed to investigate the clinicopathologic and molecular features of pure SBC.

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Breast carcinoma (multi t Breast carcinoma (multi t Breast carcinoma (multi t Breast carcinoma (combina Breast carcinoma (combina Breast invasive ductal ca Breast cancer tissue arra Breast cancer and matched Breast cancer and matched Tissue array of breast ca Breast cancer and matched Breast cancer and matched

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p53 mutation regulates PKD genes and results in co-occurrence of PKD and tumorigenesis.

Polycystic kidney disease (PKD) is the major cause of kidney failure and mortality in humans. It has always been suspected that the development of cystic kidney disease shares features with tumorigenesis, although the evidence is unclear.

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Salvianolic Acid B Attenuates Apoptosis of HUVEC Cells Treated with High Glucose or High Fat via Sirt1 Activation.

High glucose and high fat are important inducements for the development and progression of diabetic cardiopathy. Salvianolic acid B (SAB), which is the most abundant and bioactive compound in Danshen, attenuates oxidative stress-related disorders, such as cardiovascular diseases, cerebral ischemia, and diabetes. However, the effect of SAB on diabetic cardiopathy is not clear. The aim of study was to investigate the effect and the underlying molecular mechanisms of SAB on diabetic cardiopathy in vitro model. The human umbilical vein endothelial (HUVEC) cells were treated with high glucose (HG, 30 mM) or high fat (palmitic acid, PA, 0.75 mM) in the presence or absence of SAB (100, 200, and 400 mg/L) and incubated for 24 h. We found that HG or PA induced apoptosis of HUVEC cells, while treatment with SAB inhibited the apoptosis. We also found that SAB reversed HG- or PA-induced oxidative stress, apoptosis cell cytokines production, and expression of thioredoxin-interacting protein (TXNIP). Moreover, SAB increased HG- or PA-induced expression of Sirtuin 1 (Sirt1), a nicotinamide adenine dinucleotide- (NAD-) dependent histone deacetylase. Exposure of HUVEC cells to Ex527 (Sirt1 inhibitor) suppressed the effect of SAB on acetyl-p53 and procaspase-3 expressions. In conclusion, the results suggested that SAB could attenuate HUVEC cells damage treated with HG or PA via Sirt1 and might be a potential therapy agent for the diabetic cardiopathy treatment.

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MiR-155-5p accelerates the metastasis of cervical cancer cell via targeting TP53INP1.

The dysregulation of microRNAs has been implicated in the progression of different malignancies. Herein, we sought to identify the precise roles of miR-155-5p in the progression of cervical cancer. The expressions of miR-155-5p in cervical carcinoma cells and clinical tissues were assessed using qRT-PCR analysis. The functions of miR-155-5p on the growth of cervical cancer cell were investigated using MTT and colony formation. The Transwell and wound closure assays were selected to explore the influence of miR-155-5p on the invasion and migration of cervical cancer cell. The effect of miR-155-5p on cervical carcinoma cell growth and metastasis in vivo was investigated using xenograft model and experimental lung metastasis model. Bioinformatics analysis and luciferase reporter assay were applied to identify that tumor protein p53-inducible nuclear protein 1 (TP53INP1) was the target of miR-155-5p. MiR-155-5p was significantly upregulated in cervical cancer tissue than that in control normal tissue. Downexpression of miR-155-5p decreased the growth, migration as well as invasiveness abilities of cervical cancer cell in vitro whereas overregulation of miR-155-5p caused the opposite outcomes. In addition, the in vivo mice xenograft model suggested that downexpression of miR-155-5p restrained the progression of cervical cancer cell whereas overexpression of miR-155-5p caused opposite outcomes. Furthermore, we revealed that TP53INP1 was the target of miR-155-5p and the level of TP53INP1 was inversely associated with miR-155-5p level in cervical carcinoma. Furthermore, TP53INP1 knockdown mimicked the influence of miR-155-5p on cervical cancer proliferation, migration and invasion phenotypes. Finally, overexpression of TP53INP1 impaired the promote effect of miR-155-5p on cervical cancer cell and downregulation of TP53INP1 counteracted the suppressive impact of miR-155-5p on the aggressiveness of cervical cancer cell. Our study indicated that miR-155-5p regulated the development of cervical cancer cell by regulating the expression of TP53INP1.

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Cell Meter™ Cell Viabil Cell Meter™ Cell Viabil Cell Meter™ Cell Viabil Cell Meter™ Cell Viabil Cell Meter™ Cell Viabil Rat Mesenchymal Cells anti CD7 All T cells Reco anti Transferrin receptor OGG1 Knock Down Cell Line Cervical cancer and norma Mid advanced stage bladde Breast cancer tissue arra

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Epigenetic regulation of ferroptosis by H2B monoubiquitination and p53.

Monoubiquitination of histone H2B on lysine 120 (H2Bub1) is an epigenetic mark generally associated with transcriptional activation, yet the global functions of H2Bub1 remain poorly understood. Ferroptosis is a form of non-apoptotic cell death characterized by the iron-dependent overproduction of lipid hydroperoxides, which can be inhibited by the antioxidant activity of the solute carrier family member 11 (SLC7A11/xCT), a component of the cystine/glutamate antiporter. Whether nuclear events participate in the regulation of ferroptosis is largely unknown. Here, we show that the levels of H2Bub1 are decreased during erastin-induced ferroptosis and that loss of H2Bub1 increases the cellular sensitivity to ferroptosis. H2Bub1 epigenetically activates the expression of SLC7A11. Additionally, we show that the tumor suppressor p53 negatively regulates H2Bub1 levels independently of p53's transcription factor activity by promoting the nuclear translocation of the deubiquitinase USP7. Moreover, our studies reveal that p53 decreases H2Bub1 occupancy on the SLC7A11 gene regulatory region and represses the expression of SLC7A11 during erastin treatment. These data not only suggest a noncanonical role of p53 in chromatin regulation but also link p53 to ferroptosis via an H2Bub1-mediated epigenetic pathway. Overall, our work uncovers a previously unappreciated epigenetic mechanism for the regulation of ferroptosis.

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Monitoring flux in signalling pathways through measurements of 4EBP1-mediated eIF4F complex assembly.

The most commonly occurring cancer mutations, including oncogenes such as MYC, Ras and PIK3C, are found in signal transductions pathways feeding into the translational machinery. A broad range of translation initiation factors are also commonly found to be either amplified or mis-regulated in tumours, including eIF4E (elongation initiation factor 4E). eIF4E is a subunit of the eIF4F protein initiation complex and required for its recruitment. Here we measure the formation of the eIF4F complex through interactions of eIF4E and eIF4G subunits, and the effect of oncogenic signalling pathways on complex formation.

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