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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.
Hodgkin Lymphoma
Published in Tariq I. Mughal, Precision Haematological Cancer Medicine, 2018
There are distinct histological, genotypic and immunophenotypic features between the Hodgkin/Reed–Sternberg (HRS) cell in cHL, and the malignant cell in NLPHL, known as the lymphocyte predominant (LP) cell. The LP cell has a ‘popcorn’ appearance, strongly expresses B-cell markers, is usually negative for EBV and mutations of SGK1, DUSP2 and JUNB play an important role in the molecular pathogenesis. These genetic features are epitomize the clonal relatedness of NLPHL and DLBCL (Figures 10.4 and 10.5). Additionally, there are differences in the composition of the microenvironment’s inflammatory cells, with LP cells being surrounded by rosetting follicular helper T-cells (CD3, CD4, CD57 and PD-1 positive) and HRS cells with large number of reactive B- and T-cells (T-helper, T-regulatory and cytotoxic T-cells), histiocytes, plasma cells, eosinophils and neutrophils.
The beneficial effect of salubrinal on neuroinflammation and neuronal loss in intranigral LPS-induced hemi-Parkinson disease model in rats
Published in Immunopharmacology and Immunotoxicology, 2022
Fatma Nihan Cankara, Meliha Sümeyye Kuş, Caner Günaydın, Sinan Şafak, Süleyman Sırrı Bilge, Ozlem Ozmen, Emine Tural, Arjan Kortholt
Previous studies have shown that salubrinal inhibits the PP1 phosphatase which results in increased eIF2α phosphorylation and chondroprotective effects [43]. The antiapoptotic action of salubrinal was shown to be mediated via the eIF2α-ATF4-CHOP signaling pathway [15]. Furthermore, recent studies revealed that salubrinal lowers the expression of PP1 and DUSP2 [43]. DUSP2 is a MAPK phosphatase that is predominantly expressed in immune cells, where it regulates cytokine release during inflammation [44]. PP1 regulates eIF2α phosphorylation thereby inducing apoptosis via the eIF2α-ATF4-CHOP pathway. Consistent with these studies our data show that salubrinal suppressed the LPS-stimulated PP1and DUSP2 expression. Our data thus suggests that salubrinal regulates neuroinflammation and neuronal cell death via the PP1 and DUSP2 pathway.
Role and molecular mechanism of stem cells in colorectal cancer initiation
Published in Journal of Drug Targeting, 2020
Meng-Yan Wang, Yu-Han Qiu, Mei-Lian Cai, Cong-Hui Zhang, Xiao-Wei Wang, Hong Liu, Yi- Chen, Wu-Li Zhao, Jing-Bo Liu, Rong-Guang Shao
In recent years, scientists have discovered a negative correlation between the dual-specificity phosphatase 2 (DUSP2) and the CSC phenotype [70]. The ERK pathway has been shown to play an important role in the maintenance of CSC phenotypes [71]. Scientists isolated primary CD133 high and CD133 low cells from patients with colorectal cancer. The results from the experiment revealed that enhanced ERK activation was observed in CD133 high cells compared to CD133 low cells. This finding proved that ERK activation was critical for the maintenance of tumour stem cells and the proliferation of tumours. As a phosphatase, DUSP2 mediated dephosphorylation of ERK, thereby interrupting the proliferation of cancer cells and disrupting the maintenance of tumour stem cell characteristics [70].
DUSP2 regulates extracellular vesicle-VEGF-C secretion and pancreatic cancer early dissemination
Published in Journal of Extracellular Vesicles, 2020
Chu-An Wang, I-Heng Chang, Pei-Chi Hou, Yu-Jing Tai, Wan-Ning Li, Pei-Ling Hsu, Shang-Rung Wu, Wen-Tai Chiu, Chien-Feng Li, Yan-Shen Shan, Shaw-Jenq Tsai
Constitutive activation of MAPK pathway was characterized as one of the features of pancreatic cancer [7]. In a genetic mouse model of pancreatic cancer, MAPK signalling is required to initiate and maintain the pancreatic intraepithelial neoplasia lesions [8]. In normal cells, MAPKs mediated signalling is crucial to various cell functions. Activation of MAPKs is counteracted by dual-specificity phosphatases (DUSPs) [9]. DUSPs are unique protein phosphatases which dephosphorylate both tyrosine and serine/threonine residues on the same substrate [10]. DUSP2, also known as phosphatase of activated cells 1, belongs to the subfamily that predominantly acts in the nucleus and primarily inactivates ERK [11–14]. DUSP2 expresses mainly in the haematopoietic cells and is highly inducible in response to stress and regulates cytokine production or inflammation [15]. In cancer cells, DUSP2 was identified as a transcriptional target of p53, which mediates oxidative damage and nutritional stress-induced apoptosis [16]. Downregulation of DUSP2 and constitutive activation of ERK were detected in acute leukaemia and some solid tumours [17,18], suggesting DUSP2 may have a tumour suppressor function. Previously, we demonstrated that DUSP2 was suppressed by hypoxia and the reduction of DUSP2 contributed to tumour malignancy and drug resistance [18–20]. Considering the early dissemination nature of PDAC and tumour suppressor function of DUSP2, it is important to investigate the pathological effect of DUSP2 in pancreatic cancer progression and to dissect the underlying mechanism.