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Toxic Effects and Biodistribution of Ultrasmall Gold Nanoparticles *
Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Gunter Schmid, Wolfgang G. Kreyling, Ulrich Simon
Pan et al. pointed out that for Au1.4MS and Au15MS, the major cell-death pathway is oxidative stress [58]. All indicators of oxidative stress, reactive oxygen species (ROS), mitochondrial potential and integrity, and mitochondrial substrate reduction are compromised. In addition, they performed mRNA expression analysis using Affymetrix gene chips. The results are illustrated in Fig. 15.17. In a so-called heat map presentation, it is illustrated that a group of growth-related genes (PTGER4, EDN1, NR4A1, C5orf13, NR4A3, EGR3, FOS, EMP1, CALD1, SERPINE1, EGR1, DUSP5, ATF3, DUSP2) were upregulated in HeLa cells treated with both Au1.4MS (the signature of these particles is “s”: small) and Au15MS (the signature of these particles is “b”: big) at 1 h after the onset of treatment (s1h_1, s1h_2, b1h_1, b1h_2). This reflected an initial growth response triggered by addition of fresh media along with the Au1.4MS and Au15MS, which illustrates a well-known short-term phenomenon of cell culture and confirms the validity of the gene chip expression study. A separate clustering of the gene expression changes following treatment with the non-toxic Au15MS confirmed an overlapping, almost identical group of genes (EGR1, NR4A1, DUSP5, PPP1R3B, EDN1, FOS, EGR1, EDN1, ADAMTS1, ATF3, PTGER4, CYR61) as upregulated at 1 h after medium exchange irrespective of toxicity.
Molecular Diagnostic Approaches in Infectious Disease
Published in Attila Lorincz, Nucleic Acid Testing for Human Disease, 2016
Leonard F. Peruski, Anne Harwood Peruski
For example, when examining host response to infection with intracellular C. pneumoniae, C. trachomatis, and S. typhimurium pathogens, distinct expression profiles could be detected, demonstrating the ability to characterize pathogenic agents via host profile analysis.158 C. trachomatis and C. pneumoniae infection induced CTGF, ETV4, NR4A2, DUSP4, DUSP5, GAS-1, EGR1 LIF, MIP-2, IER3, MCL-1, EPHA2, IL6, and IL8. C. trachomatis induced IL-11 Gro-alpha, GM-CSF, and fos-related antigen FRA- 1, while C. pneumoniae induced IL-8, ICAM-1, and prostaglandin endoperoxide-synthase 2 (Cox 2, PTGS2). Intracellular Salmonella infection caused major increases in IL-6 and IL-8 mRNA levels only.
Functional Mechanism of MicroRNA-25-3p in Hilar Cholangiocarcinoma Cell Proliferation and Migration Through Regulation of Dual Specificity Phosphatase 5
Published in Journal of Investigative Surgery, 2023
Wan Zhong, Shiyang Dong, Han Wang, Chao Pan, Shiyong Yang
Out of 999 DEGs from GSE34166 datasets and 125 DEGs from GSE68292 dataset, we managed to identify 15 intersection DEGs that might be associated with HCCA. Among these genes, DUSP5 is considered a direct transcriptional target of tumor suppressor p53.25 Additionally, DUSP5 exhibits low expression patterns in Hodgkin’s lymphoma cells and other tumor cells from hematopoietic and non-hematopoietic malignancies relative to nonmalignant cells.26 Thereby, we hypothesized the same mechanism of DUSP5 in HCCA and selected DUSP5 as the study subject. miR-25-3p is a member of the known oncogenic miR-25-93-106b cluster.27 Starbase database reveals high expression of miR-25-3p in HCCA. Moreover, bioinformatics analysis showed high expression of miR-25-3p and low expression of DUSP5 in HCCA. The same expression patterns were observed in the FRH-0201 cells we cultured in vitro. Our results elucidated that miR-25-3p targeted DUSP5 in HCCA, evidenced by the decreased DUSP5 levels after miR-25-3p overexpression and increased levels of DUSP5 after miR-25-3p knockdown. Previous findings elicited that DUSP5 is the target gene of miR-95 and miR-203,21,28 the expression patterns and functions of which in HCCA remain elusive and require in-depth investigation in the future.
Dysregulation of lncRNA-H19 in cardiometabolic diseases and the molecular mechanism involved : a systematic review
Published in Expert Review of Molecular Diagnostics, 2021
Ana Iris Hernández-Aguilar, Carlos Aldair Luciano-Villa, Vianet Argelia Tello-Flores, Fredy Omar Beltrán-Anaya, Ma Isabel Zubillaga-Guerrero, Eugenia Flores-Alfaro
Decreased levels of H19 have been reported in the muscles of both patients with T2D and insulin-resistant mice, which leads to increased bioavailability of let-7, which in turn inhibits the expression of key metabolic genes such as insulin receptor and lipoprotein lipase [92]. On the other hand, it has been reported that H19 posttranscriptionally regulates DUSP5 expression by reducing the bioavailability of let-7. DUSP5 is highly expressed in the muscles and activates AMPK in muscle cells. A decrease in DUSP5 reduces the phosphorylation of AMPK, which leads to decreased glucose uptake and altered fatty acid biosynthesis by activating PGC-1α and inactivating acetyl-CoA carboxylase [93]. Thus, H19 could positively regulate adenosine monophosphate-activated protein kinase (AMPK) activity through the let-7/DUSP5 pathway, in such a manner that a decrease in H19 expression is strongly associated with a decrease in glucose uptake and IR in the muscle cells.
Simvastatin suppresses renal cell carcinoma cells by regulating DDX5/DUSP5
Published in Scandinavian Journal of Urology, 2021
Yu Qiu, Yakun Zhao, Haipng Wang, Wei Liu, Chengluo Jin, Wanhai Xu
First, we explored the expression of DDX5 in HK-2, A498 and ACHN cells. Compared with HK-2 cells, expression of DDX5 was increased in A498 and ACHN cells, as determined by immunofluorescence (Figure 4(a)). The opposite was observed with DUSP5, which was inhibited in RCC cells, supporting our hypothesis. Following treatment of A498 and ACHN cells with si-NC + 2.5 μM simvastatin, migration and invasion were inhibited, as revealed by wound healing and Transwell assays (Figures 4(b and c)). However, siRNA targeting DUSP5 reversed the simvastatin-mediated suppression of migration and invasion. To investigate the underlying mechanism, we determined the protein expression of DUSP5 and DDX5 after inhibiting DUSP5 via siRNA. In the control group, DDX5 was upregulated and DUSP5 was downregulated. Thus, our results suggest that DDX5 can negatively regulate DUSP5. Following treatment with simvastatin, the expression of DDX5 and DUSP5 was reversed compared with the control group. Thus, simvastatin might exert its inhibitory actions via DDX5/DUSP5. To further confirm this, we used RNA interference to suppress the expression of DUSP5. As expected, the protein expression of both DDX5 and DUSP5 nearly returned to control levels when treated with simvastatin + DUSP5 siRNA in the two cell lines (Figure 4(D)). These data confirmed that simvastatin suppressed migration and invasion of A498 and ACHN cells by regulating DDX5/DUSP5.