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Description
flow cytometer, flow cytometer, flow cytometer, flow cytometer, cytometer
This model was found at
1628 locations
The model is used in
53 countries
Usage per year (up to 2020)
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143 related research fields
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About the Beckman Coulter Cytomics

The model Beckman Coulter Cytomics was found in 1628 unique locations in 53 countries where it was mentioned from 2002 until recentlyIt is used by scientists in various research fields such as General Medicine, Oncology, Cancer Research, Molecular Biology, and Immunology. The model is also used in Molecular Medicine, Immunology and Allergy, Biochemistry, Pharmacology, Genetics, Cell Biology, Organic Chemistry, General Biochemistry, Genetics and Molecular Biology, Pharmaceutical Science, Drug Discovery, Physical and Theoretical Chemistry, General Chemistry, Hematology, Biotechnology, Catalysis, Infectious Diseases, Biomedical Engineering, Cellular and Molecular Neuroscience, Bioengineering, Inorganic Chemistry, Pharmacology (medical), Computer Science Applications, Medicine, Analytical Chemistry, and Physiology.
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Research that uses the Beckman Coulter Cytomics

Jiemin Ding, Min Liu, Zihua Xuan, Meng li Liu, Ning Wang, Xiaoyi Jia, Evidence-Based Complementary and Alternative Medicine, 2020, 1-10, 2020
Aims. The aim of this study was to evaluate the protective effects of Er Miao San (EMS) and the regulative function of bone marrow-derived dendritic cells (BMDCs) on adjuvant arthritis (AA) in rats. Methods. The ethyl acetate part of EMS (3 g/kg, 1.5 g/kg, and 0.75 g/kg) was orally administered from day 15 after immunization to day 29. The polyarthritis index and paw swelling were measured, the ankle joint pathological changes were observed using hematoxylin-eosin (HE) staining, and the spleen and thymus index were determined. Moreover, T and B cell proliferation were determined using the CCK-8 assay. The expression of BMDC surface costimulatory molecules and inflammatory factors were determined using flow cytometry and ELISA kits, respectively. Results. Compared with the AA model rats, the ethyl acetate fraction of EMS obviously reduced paw swelling (from 1.0 to 0.7) and the polyarthritis index (from 12 to 9) P < 0.01 and improved the severity of histopathology P < 0.01 . The treatment using ethyl acetate fraction of EMS significantly reduced the spleen and thymus index P < 0.01 and inhibited T and B cell proliferation P < 0.01 . Moreover, EMS significantly modulated the expression of surface costimulatory molecules in BMDCs, including CD40, CD80, CD86, and major histocompatibility complex class II (MHC-II) P < 0.01 . The results also showed that the ethyl acetate part of EMS significant inhibited the levels of proinflammatory cytokines interleukin- (IL-) 23 tumor necrosis factor- (TNF-) α and inflammatory factor prostaglandin (PG) E2 in the supernatant of BMDCs. However, the level of anti-inflammatory cytokine IL-10 was significantly increased P < 0.01 . Conclusion. These results suggest that the ethyl acetate part of EMS has better protective effects on AA rats, probably by regulating the function of BMDCs and modulating the balance of cytokines.
Rahmat Dani Satria, Tzu-Wen Huang, Ming-Kai Jhan, Ting-Jing Shen, Po-Chun Tseng, Yun-Ting Wang, Zhen-Yu Yang, Chung-Hsi Hsing, Chiou-Feng Lin, Journal of Immunology Research, 2021, 1-10, 2021
During the acute febrile phase of dengue virus (DENV) infection, viremia can cause severe systemic immune responses accompanied by hematologic disorders. This study investigated the potential induction and mechanism of the cytopathic effects of DENV on peripheral blood cells ex vivo. At one day postinfection, there was viral nonstructural protein NS1 but no further virus replication measured in the whole blood culture. Notably, DENV exposure caused significant vacuolization in monocytic phagocytes. With a minor change in the complete blood cell count, except for a minor increase in neutrophils and a significant decrease in monocytes, the immune profiling assay identified several changes, particularly a significant reduction in CD14-positive monocytes as well as CD11c-positive dendritic cells. Abnormal production of TNF-α was highly associated with the induction of vacuolization. Manipulating TNF-α expression resulted in cytopathogenic effects. These results demonstrate the potential hematological damage caused by ex vivo DENV-induced TNF-α.
Qikui Wu, Zihan Zhang, Huan Peng, Yali Wu, Fangyuan Yu, PeerJ, 7, e7996, 2019
Background Styrax tonkinensis is a great potential biofuel as the species contains seeds with a particularly high oil content. Understanding the nutrient distribution in different parts of the fruit is imperative for the development and enhancement of S. tonkinensis as a biodiesel feedstock. Methods From 30 to 140 days after flowering (DAF), the development of S. tonkinensis fruit was tracked. The morphology change, nutrient content, and activity of associated enzymes in the continuum of the pericarp, seed coat, and kernel were analyzed. Results Between 30 and 70 DAF, the main locus of dry matter deposition shifted from the seed coat to the kernel. The water content within the pericarp remained high throughout development, but at the end (130 DAF later) decreased rapidly. The water content within both the seed coat and the kernel consistently declined over the course of the fruit development (30–110 DAF). Between 70 and 80 DAF, the deposition centers for sugar, starch, protein, potassium, and magnesium was transferred to the kernel from either the pericarp or the seed coat. The calcium deposition center was transferred first from pericarp to the seed coat and then to the kernel before it was returned to the pericarp. The sucrose to hexose ratio in the seed coat increased between 30 and 80 DAF, correlating with the accumulation of total soluble sugar, starch, and protein. In the pericarp, the sucrose to hexose ratio peaked at 40 and 100 DAF, correlating with the reserve deposition in the following 20–30 days. After 30 DAF, the chlorophyll concentration of both the pericarp and the seed coat dropped. The maternal unit (the pericarp and the seed coat) in fruit showed a significant positive linear relationship between chlorophyll b/a and the concentration of total soluble sugar. The potassium content had significant positive correlation with starch (ρ = 0.673, p = 0.0164), oil (ρ = 0.915, p = 0.000203), and protein content (ρ = 0.814, p = 0.00128), respectively. The concentration of magnesium had significant positive correlation with starch (ρ = 0.705, p = 0.0104), oil (ρ = 0.913, p = 0.000228), and protein content (ρ = 0.896, p = 0.0000786), respectively. Calcium content had a significant correlation with soluble sugar content (ρ = 0.585, p = 0.0457). Conclusions During the fruit development of S. tonkinensis, the maternal unit, that is, the pericarp and seed coat, may act a nutrient buffer storage area between the mother tree and the kernel. The stage of 70–80 DAF is an important time in the nutrient distribution in the continuum of the pericarp, seed coat, and kernel. Our results described the metabolic dynamics of the continuum of the pericarp, seed coat, and kernel and the contribution that a seed with high oil content offers to biofuel.
Lei Zhao, Wei Chen, Guoliang Qiao, Jiangping Wu, Duo Yang, Xiaoli Wang, Xinna Zhou, Shuo Wang, Jun Ren, 2020
Abstract Background Our understanding of sepsis-associated immune impairment is incomplete. The objective of this retrospective study was to investigate correlations of sepsis clinical manifestations with peripheral blood lymphocyte subpopulations in lymphocyte immunity. Methods Twenty individuals without sepsis and eighteen with sepsis were enrolled. Lymphocyte phenotypes (CD3+, CD4+, CD8+, CD3-CD16+CD56+, CD19+, CD4+CD25+CD127+, CD8+CD28-, and CD8+CD28+) were assessed by flow cytometry. Fresh fecal bacteria cue proportion was measured to determine intestinal dysbacteriosis. Results Compared with the non-sepsis group, the sepsis patients had clearly lower proportions of CD3+, CD4+ and CD8+CD28+ cells and substantially higher proportions of CD19+ cells (p<0.05). Among 38 patients with infection, CD4+ cells and CD8+CD28+ cells in a survivor group had significantly higher presence compared with patients who had died (p<0.05), The subgroup analysis results showed that CD4+ cells in the survivor subgroups were higher than those in the deceased subgroups (p<0.05). CD8+CD28+ cells in the non-sepsis survivor subgroup were higher than those in the deceased subgroups (p<0.05).. Bivariate correlation analysis showed that the intestinal dysbacteriosis was significantly correlated with the severity of sepsis and its prognosis (r2=0.2788, p=0.001, r2=0.1764, p=0.009, respectively). CD4+, CD19+, and CD8+CD28+ cells were significantly correlated with intestinal dysbacteriosis (r2=0.1024, p=0.049, r2=0.1063, p=0.046, r2=0.1909, p=0.006, respectively). Conclusions In conclusion, the lymphocyte populations of CD3+, CD4+, CD8+CD28+ and CD19+ cells were accessible for predicting the severity and mortality of sepsis patients. In addition, intestinal dysbacteriosis had a significant impact on the immune system of sepsis patients as revealed by peripheral blood lymphocyte population.
Yan-chun Qu, Ying Zou, Shuai Shi, Yanjuan Zhu, Yi-hong Liu, Li-rong Liu, Xiao-hua Zheng, Hui-hui Chen, Hai-bo Zhang, 2020
Abstract Background: Traditional Chinese Medicine (TCM) prescriptions should be decided according to the TCM treatment principle, and the warming-yang or cooling-heat should be the guide of treatment principle outline. Methods: In order to identify which treatment principle, warming-yang or cooling-heat should be combined with epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in non-small cell lung cancer (NSCLC), we combined the typical warming-yang drug, Shen-fu (SF), and the typical cooling-heat drug, Qing-kai-ling (QKL) with gefitinib in resistant NSCLC models. Results: The results demonstrated that QKL combined with gefitinib induced significantly increased cell viability inhibition and apoptosis in A549 cell line and significantly smaller tumor volume and lower tumor weight in H1975 xenograft transplanted nude mice. On the contrary, SF combined with gefitinib had significant antagonism effect on both cell viability inhibition and apoptosis in vitro , and on tumor weight in vivo . EGFR phosphorylation inhibition and the downstream PI3K/AKT and RAS/RAF/ERK pathway inhibition served an important role in the synergism effect between QKL and gefitinib in H1975 xenograft transplanted nude mice. Conclusions: The present study indicated that cooling-heat TCM treatment principle may reverse or delay NSCLC resistance to EGFR-TKIs, and combination of them warrants further study.
Weiguo Lao, Yi Tan, Michael Johnson, Yan Li, Yiguang Lin, Linda Xiao, Xianqin Qu, 2020
Abstract Background: Osteoporosis is a metabolic disease affecting the bone mineral density associated with increased adiposity in the aging population with obesity. The nutrients to control osteoblast and adipocyte differentiation from a common precursor, the pluripotent mesenchymal stem cell (MSC), may be a promising therapy for osteoporosis. Previously, we have shown that green tea polyphenols (GTP) exert anti-adipogenic effects on preadipocyte proliferation. In the present study, we investigated regulatory effects of GTP on osteogenesis and adipogenesis during early differentiation of human adipose tissue-derived stem cells (hADSCs). Methods: GTP at concentrations of 1 and 10 µg/ml was incubated with primary hADSCs in presence or absence of pioglitazone (100 µmol) during hADSCs differentiation. Adipogenesis of hADSCs was determined by Oil Red O staining and measurement of the cellular triglyceride synthesis in mature adipocyte. Alkaline phosphatase (ALP) assay and the measurement of intracellular calcium were utilized to determine osteoporosis of hADSCs. Immunofluorescence staining and qRT-PCR were employed to detect PPARγ-CEBPA regulated adipogenic pathway and the RUNX2-BMP2 mediated osteogenic pathway. Results: GTP treatment significantly decreased lipid accumulation and the cellular triglyceride synthesis in mature adipocytes and attenuated pioglitazone-induced adipogenesis in a dose-dependent manner. GTP downregulated protein and mRNA expression of Pparγ and attenuated pioglitazone-stimulated Cebpa expression in mature adipocytes. Concurrently, measurements of calcium content and ALP activity showed that GTP treatment significantly enhanced hADSCs differentiation into osteocytes compared with the control and pioglitazone-treated cells. Meanwhile, GTP upregulated protein and mRNA expression of RunX2 and Bmp2 compared to the control and GTP at 10 µg/mL significantly attenuated the decreased mRNA expression of Runx2 and Bmp2 by pioglitazone. Conclusions: The present study demonstrated that GTP possess a greater ability to facilitate osteogenesis and simultaneously inhibit hADSCs differentiation into the adipogenic lineage through upregulating the RUNX2-BMP2 mediated osteogenic pathway and suppressing PPARγ-induced signaling of adipogenesis. The findings of this study highlight that GTP may be a therapeutic intervention to combat osteoporosis associated obesity.
Abel D. Ang, Margreet C. M. Vissers, Eleanor R. Burgess, Margaret J. Currie, Gabi U. Dachs, Antioxidants, 10, 430 (3), 2021
Tumour-associated macrophages (TAMs) are ubiquitously present in tumours and commonly associated with poor prognosis. In immune cells, ascorbate affects epigenetic regulation, differentiation and phenotype via its co-factor activity for the 2-oxoglutarate dependent dioxygenase enzymes. Here, we determined the effect of ascorbate on TAM development in response to tumour microenvironmental cues. Naïve murine bone marrow monocytes were cultured with Lewis Lung Carcinoma conditioned media (LLCM) or macrophage colony-stimulating factor (MCSF) to encourage the development into tumour-associated macrophages. Cells were stimulated with hypoxia (1% O2), with or without ascorbate (500 µM) supplementation. Cells and media were harvested for gene, cell surface marker and protein analyses. LLCM supported bone marrow monocyte growth with >90% of cells staining CD11b+F4/80+, indicative of monocytes/macrophages. LLCM-grown cells showed increased expression of M2-like and TAM genes compared to MCSF-grown cells, which further increased with hypoxia. In LLCM-grown cells, ascorbate supplementation was associated with increased F4/80 cell surface expression, and altered gene expression and protein secretion. Our study shows that ascorbate modifies monocyte phenotype when grown under tumour microenvironmental conditions, but this was not clearly associated with either a pro- or anti-tumour phenotype, and reflects a complex and nuanced response of macrophages to ascorbate. Overall, ascorbate supplementation clearly has molecular consequences for TAMs, but functional and clinical consequences remain unknown.
Zaida Abad-Jiménez, Sandra López-Domènech, Segundo Ángel Gómez-Abril, Dolores Periañez-Gómez, Aranzazu M. de Marañón, Celia Bañuls, Carlos Morillas, Víctor M. Víctor, Milagros Rocha, Antioxidants, 9, 734 (8), 2020
Little is known about the mechanisms underlying the cardioprotective effect of Roux en-Y gastric bypass (RYGB) surgery. Therefore, the aim of the present study was to investigate whether weight loss associated with RYGB improves the oxidative status of leukocytes and ameliorates subclinical atherosclerotic markers. This is an interventional study of 57 obese subjects who underwent RYGB surgery. We determined biochemical parameters and qualitative analysis of cholesterol, leukocyte and systemic oxidative stress markers —superoxide production, glutathione peroxidase 1 (GPX1), superoxide dismutase (SOD) activity and protein carbonylation—, soluble cellular adhesion molecules —sICAM-1 and sP-selectin—, myeloperoxidase (MPO) and leukocyte-endothelium cell interactions—rolling flux, velocity and adhesion. RYGB induced an improvement in metabolic parameters, including hsCRP and leukocyte count (p < 0.001, for both). This was associated with an amelioration in oxidative stress, since superoxide production and protein carbonylation were reduced (p < 0.05 and p < 0.01, respectively) and antioxidant systems were enhanced (GPX1; p < 0.05 and SOD; p < 0.01). In addition, a significant reduction of the following parameters was observed one year after RYGB: MPO and sICAM (p < 0.05, for both), sPselectin and pattern B of LDL particles (p < 0.001, for both), and rolling flux and adhesion of leukocytes (p < 0.05 and p < 0.01, respectively). Our results suggest that patients undergoing RYGB benefit from an amelioration of the prooxidant status of leukocytes, metabolic outcomes, and subclinical markers of atherosclerosis.
Leticia Pollo-Oliveira, Roland Klassen, Nick Davis, Akif Ciftci, Jo Bacusmo, Maria Martinelli, Michael DeMott, Thomas Begley, Peter Dedon, Raffael Schaffrath, Valérie de Crécy-Lagard, Biomolecules, 10, 322 (2), 2020
Modifications found in the Anticodon Stem Loop (ASL) of tRNAs play important roles in regulating translational speed and accuracy. Threonylcarbamoyl adenosine (t6A37) and 5-methoxycarbonyl methyl-2-thiouridine (mcm5s2U34) are critical ASL modifications that have been linked to several human diseases. The model yeast Saccharomyces cerevisiae is viable despite the absence of both modifications, growth is however greatly impaired. The major observed consequence is a subsequent increase in protein aggregates and aberrant morphology. Proteomic analysis of the t6A-deficient strain (sua5 mutant) revealed a global mistranslation leading to protein aggregation without regard to physicochemical properties or t6A-dependent or biased codon usage in parent genes. However, loss of sua5 led to increased expression of soluble proteins for mitochondrial function, protein quality processing/trafficking, oxidative stress response, and energy homeostasis. These results point to a global function for t6A in protein homeostasis very similar to mcm5/s2U modifications.
Preethi Vetrivel, Seong Min Kim, Sang Eun Ha, Hun Hwan Kim, Pritam Bhagwan Bhosale, Kalaiselvi Senthil, Gon Sup Kim, Biomolecules, 10, 1086 (7), 2020
Gastric cancer is the common type of malignancy positioned at second in mortality rate causing burden worldwide with increasing treatment options. Prunetin (PRU) is an O-methylated flavonoid that belongs to the group of isoflavone executing beneficial activities. In the present study, we investigated the anti-proliferative and cell death effect of the compound PRU in AGS gastric cancer cell line. The in vitro cytotoxic potential of PRU was evaluated and significant proliferation was observed. We identified that the mechanism of cell death was due to necroptosis through double staining and was confirmed by co-treatment with inhibitor necrostatin (Nec-1). We further elucidated the mechanism of action of necroptosis via receptor interacting protein kinase 3 (RIPK3) protein expression and it has been attributed by ROS generation through JNK activation. Furthermore, through computational analysis by molecular docking and dynamics simulation, the efficiency of compound prunetin against RIPK3 binding was validated. In addition, we also briefed the pharmacokinetic properties of the compound by in silico ADMET analysis.
Ibtesam R. T. Al Delfi, Chelsea R. Wood, Louis D. V. Johnson, Martyn D. Snow, John F. Innes, Peter Myint, William E. B. Johnson, Biomolecules, 10, 1301 (9), 2020
The majority of research into the effects of mesenchymal stem cell (MSC) transplants on spinal cord injury (SCI) is performed in rodent models, which may help inform on mechanisms of action, but does not represent the scale and wound heterogeneity seen in human SCI. In contrast, SCI in dogs occurs naturally, is more akin to human SCI, and can be used to help address important aspects of the development of human MSC-based therapies. To enable translation to the clinic and comparison across species, we have examined the paracrine, regenerative capacity of human and canine adipose-derived MSCs in vitro. MSCs were initially phenotyped according to tissue culture plastic adherence, cluster of differentiation (CD) immunoprofiling and tri-lineage differentiation potential. Conditioned medium (CM) from MSC cultures was then assessed for its neurotrophic and angiogenic activity using established cell-based assays. MSC CM significantly increased neuronal cell proliferation, neurite outgrowth, and βIII tubulin immunopositivity. In addition, MSC CM significantly increased endothelial cell migration, cell proliferation and the formation of tubule-like structures in Matrigel assays. There were no marked or significant differences in the capacity of human or canine MSC CM to stimulate neuronal cell or endothelial cell activity. Hence, this study supports the use of MSC transplants for canine SCI; furthermore, it increases understanding of how this may subsequently provide useful information and translate to MSC transplants for human SCI.
Eva Pokorná, Tomáš Hluska, Petr Galuszka, H. Tucker Hallmark, Petre I. Dobrev, Lenka Záveská Drábková, Tomáš Filipi, Katarína Holubová, Ondřej Plíhal, Aaron M. Rashotte, Roberta Filepová, Jiří Malbeck, Ondřej Novák, Lukáš Spíchal, Břetislav Brzobohatý, Pavel Mazura, Lenka Zahajská, Václav Motyka, Biomolecules, 11, 24 (1), 2020
Cytokinins (CKs) are a class of phytohormones affecting many aspects of plant growth and development. In the complex process of CK homeostasis in plants, N-glucosylation represents one of the essential metabolic pathways. Its products, CK N7- and N9-glucosides, have been largely overlooked in the past as irreversible and inactive CK products lacking any relevant physiological impact. In this work, we report a widespread distribution of CK N-glucosides across the plant kingdom proceeding from evolutionary older to younger plants with different proportions between N7- and N9-glucosides in the total CK pool. We show dramatic changes in their profiles as well as in expression levels of the UGT76C1 and UGT76C2 genes during Arabidopsis ontogenesis. We also demonstrate specific physiological effects of CK N-glucosides in CK bioassays including their antisenescent activities, inhibitory effects on root development, and activation of the CK signaling pathway visualized by the CK-responsive YFP reporter line, TCSv2::3XVENUS. Last but not least, we present the considerable impact of CK N7- and N9-glucosides on the expression of CK-related genes in maize and their stimulatory effects on CK oxidase/dehydrogenase activity in oats. Our findings revise the apparent irreversibility and inactivity of CK N7- and N9-glucosides and indicate their involvement in CK evolution while suggesting their unique function(s) in plants.
Valentina Giudice, Marisa Gorrese, Rosa Vitolo, Angela Bertolini, Rossella Marcucci, Bianca Serio, Roberto Guariglia, Idalucia Ferrara, Rita Pepe, Francesca D’Alto, Barbara Izzo, Antonio Pedicini, Nunzia Montuori, Maddalena Langella, Carmine Selleri, Biomedicines, 9, 387 (4), 2021
Wilm’s tumor 1 (WT1), a zinc-finger transcription factor and an epigenetic modifier, is frequently overexpressed in several hematologic disorders and solid tumors, and it has been proposed as diagnostic and prognostic marker of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). However, the exact role of WT1 in leukemogenesis and disease progression remains unclear. In this real-world evidence retrospective study, we investigated prognostic role of WT1-mRNA expression levels in AML and MDS patients and correlations with complete blood counts, flow cytometry counts, and molecular features. A total of 71 patients (AML, n = 46; and MDS, n = 25) were included in this study, and WT1 levels were assessed at diagnosis, during treatment and follow-up. We showed that WT1 expression levels were inversely correlated with normal hemopoiesis in both AML and MDS, and positively associated with blast counts. Flow cytometry was more sensitive and specific in distinguishing normal myeloid cells from neoplastic counterpart even just using linear parameters and CD45 expression. Moreover, we showed that a simple integrated approach combining blast counts by flow cytometry, FLT3 mutational status, and WT1 expression levels might be a useful tool for a better prognostic definition in both AML and MDS patients.
Elena Mariotto, Giampietro Viola, Roberto Ronca, Luca Persano, Sanja Aveic, Zaver Bhujwalla, Noriko Mori, Benedetta Accordi, Valentina Serafin, Luisa López-Cara, Roberta Bortolozzi, Cancers, 10, 391 (10), 2018
Choline kinase (ChoK) is the first enzyme of the Kennedy pathway leading to the biosynthesis of phosphatidylcholine (PtdCho), the most abundant phospholipid in eukaryotic cell membranes. EB-3D is a novel choline kinase α1 (ChoKα1) inhibitor with potent antiproliferative activity against a panel of several cancer cell lines. ChoKα1 is particularly overexpressed and hyperactivated in aggressive breast cancer. By NMR analysis, we demonstrated that EB-3D is able to reduce the synthesis of phosphocholine, and using flow cytometry, immunoblotting, and q-RT-PCR as well as proliferation and invasion assays, we proved that EB-3D strongly impairs breast cancer cell proliferation, migration, and invasion. EB-3D induces senescence in breast cancer cell lines through the activation of the metabolic sensor AMPK and the subsequent dephosphorylation of mTORC1 downstream targets, such as p70S6K, S6 ribosomal protein, and 4E-BP1. Moreover, EB-3D strongly synergizes with drugs commonly used for breast cancer treatment. The antitumorigenic potential of EB-3D was evaluated in vivo in the syngeneic orthotopic E0771 mouse model of breast cancer, where it induces a significant reduction of the tumor mass at low doses. In addition, EB-3D showed an antimetastatic effect in experimental and spontaneous metastasis models. Altogether, our results indicate that EB-3D could be a promising new anticancer agent to improve aggressive breast cancer treatment protocols.
Satendra Kumar, Hong Xie, Patrick Scicluna, Linkiat Lee, Viveca Björnhagen, Anders Höög, Catharina Larsson, Weng-Onn Lui, Cancers, 10, 443 (11), 2018
MicroRNA-375 (miR-375) is deregulated in multiple tumor types and regulates important targets involved in tumorigenesis and metastasis. This miRNA is highly expressed in Merkel cell carcinoma (MCC) compared to normal skin and other non-MCC skin cancers, and its expression is high in Merkel cell polyomavirus (MCPyV)-positive (MCPyV+) and low in MCPyV-negative (MCPyV−) MCC tumors. In this study, we characterized the function and target of miR-375 in MCPyV+ and MCPyV− MCC cell lines. Ectopic expression of miR-375 in MCPyV− MCC cells resulted in decreased cell proliferation and migration, as well as increased cell apoptosis and cell cycle arrest. However, in MCPyV+ MCC cells, inhibition of miR-375 expression reduced cell growth and induced apoptosis. Additionally, the expression of lactate dehydrogenase B (LDHB), a known target of miR-375, was inversely correlated with miR-375. Silencing of LDHB reduced cell growth in MCPyV− cell lines, while its silencing in MCPyV+ cell lines rescued the cell growth effect mediated by miR-375 inhibition. Together, our results suggest dual roles of miR-375 and LDHB in MCPyV and non-MCPyV-associated MCCs. We propose that LDHB could be a therapeutic target in MCC and different strategies should be applied in virus- and non-virus-associated MCCs.
Shang-Gin Wu, Tzu-Hua Chang, Meng-Feng Tsai, Yi-Nan Liu, Chia-Lang Hsu, Yih-Leong Chang, Chong-Jen Yu, Jin-Yuan Shih, Cancers, 11, 36 (1), 2019
Patients with epidermal growth factor receptor (EGFR) mutation-positive lung cancer show a dramatic response to EGFR-tyrosine kinase inhibitors (TKIs). However, acquired drug resistance eventually develops. This study explored the novel mechanisms related to TKI resistance. To identify the genes associated with TKI resistance, an integrative approach was used to analyze public datasets. Molecular manipulations were performed to investigate the roles of insulin-like growth factor binding protein 7 (IGFBP7) in lung adenocarcinoma. Clinical specimens were collected to validate the impact of IGFBP7 on the efficacy of EGFR TKI treatment. IGFBP7 mRNA expression in cancer cells isolated from malignant pleural effusions after acquired resistance to EGFR-TKI was significantly higher than in cancer cells from treatment-naïve effusions. IGFBP7 expression was markedly increased in cells with long-term TKI-induced resistance compared to in TKI-sensitive parental cells. Reduced IGFBP7 in TKI-resistant cells reversed the resistance to EGFR-TKIs and increased EGFR-TKI-induced apoptosis by up-regulating B-cell lymphoma 2 interacting mediator of cell death (BIM) and activating caspases. Suppression of IGFBP7 attenuated the phosphorylation of insulin-like growth factor 1 receptor (IGF-IR) and downstream protein kinase B (AKT) in TKI-resistant cells. Clinically, higher serum IGFBP7 levels and tumors with positive IGFBP7-immunohistochemical staining were associated with poor TKI-treatment outcomes. IGFBP7 confers resistance to EGFR-TKIs and is a potential therapeutic target for treating EGFR-TKI-resistant cancers.
Chia-Yang Lin, Atikul Islam, Claire J. Su, Alexander S. Tikhomirov, Andrey E. Shchekotikhin, Show-Mei Chuang, Pin Ju Chueh, Yao Li Chen, Cancers, 11, 420 (3), 2019
Hepatocellular carcinoma (HCC) is the most frequent primary malignancy of the liver and is among the top three causes of cancer-associated death worldwide. However, the clinical use of chemotherapy for HCC has been limited by various challenges, emphasizing the urgent need for novel agents with improved anticancer properties. We recently synthesized and characterized a series of 4,11-diaminoanthra[2,3-b]furan-5,10-dione derivatives that exhibit potent apoptotic activity against an array of cancer cell lines, including variants with multidrug resistance. Their effect on liver cancer cells, however, was unknown. Here, we investigated three selected 4,11-diaminoanthra[2,3-b]furan-5,10-dione derivatives (compounds 1–3) for their cytotoxicity and the underlying molecular mechanisms in wild-type or p53-deficient HCC cells. Cytotoxicity was determined by WST-1 assays and cell impedance measurements and apoptosis was analyzed by flow cytometry. The interaction between compounds and tumor-associated NADH oxidase (tNOX, ENOX2) was studied by cellular thermal shift assay (CETSA). We found that compound 1 and 2 induced significant cytotoxicity in both HepG2 and Hep3B lines. CETSA revealed that compounds 1 and 2 directly engaged with tNOX, leading to a decrease in the cellular NAD+/NADH ratio. This decreased the NAD+-dependent activity of Sirtuin 1 (SIRT1) deacetylase. In p53-wild-type HepG2 cells, p53 acetylation/activation was enhanced, possibly due to the reduction in SIRT1 activity, and apoptosis was observed. In p53-deficient Hep3B cells, the reduction in SIRT1 activity increased the acetylation of c-Myc, thereby reactivating the TRAIL pathway and, ultimately leading to apoptosis. These compounds thus trigger apoptosis in both cell types, but via different pathways. Taken together, our data show that derivatives 1 and 2 of 4,11-diaminoanthra[2,3-b]furan-5,10-diones engage with tNOX and inhibit its oxidase activity. This results in cytotoxicity via apoptosis through tNOX-SIRT1 axis to enhance the acetylation of p53 or c-Myc in HCC cells, depending on their p53 status.
Joo Young Hong, Kyung-Sook Chung, Ji-Sun Shin, Jeong-Hun Lee, Hyo-Sun Gil, Hwi-Ho Lee, Eunwoo Choi, Jung-Hye Choi, Ahmed H.E. Hassan, Yong Sup Lee, Kyung-Tae Lee, Cancers, 11, 1927 (12), 2019
We previously reported the potential anti-proliferative activity of 3-(5,6,7-trimethoxy-4-oxo-4H-chromen-2-yl)-N-(3,4,5-trimethoxyphenyl) benzamide (TMS-TMF-4f) against human cancer cells; however, the underlying molecular mechanisms have not been investigated. In the present study, TMS-TMF-4f showed the highest cytotoxicity in human cervical cancer cells (HeLa and CaSki) and low cytotoxicity in normal ovarian epithelial cells. Annexin V-FITC and propidium iodide (PI) double staining revealed that TMS-TMF-4f-induced cytotoxicity was caused by the induction of apoptosis in both HeLa and CaSki cervical cancer cells. The compound TMS-TMF-4f enhanced the activation of caspase-3, caspase-8, and caspase-9 and regulated Bcl-2 family proteins, which led to mitochondrial membrane potential (MMP) loss and resulted in the release of cytochrome c and Smac/DIABLO into the cytosol. Also, TMS-TMF-4f suppressed both constitutive and IL-6-inducible levels of phosphorylated STAT3 (p-STAT3) and associated proteins such as Mcl-1, cyclin D1, survivin, and c-Myc in both cervical cancer cells. STAT-3 overexpression completely ameliorated TMS-TMF-4f-induced apoptotic cell death and PARP cleavage. Docking analysis revealed that TMS-TMF-4f could bind to unphosphorylated STAT3 and inhibit its interconversion to the activated form. Notably, intraperitoneal administration of TMS-TMF-4f (5, 10, or 20 mg/kg) decreased tumor growth in a xenograft cervical cancer mouse model, demonstrated by the increase in TUNEL staining and PARP cleavage and the reduction in p-STAT3, Mcl-1, cyclin D1, survivin, and c-Myc expression levels in tumor tissues. Taken together, our results suggest that TMS-TMF-4f may potentially inhibit human cervical tumor growth through the induction of apoptosis via STAT3 suppression.
Jyun-Yuan Huang, Yen-Yun Wang, Steven Lo, Ling-Ming Tseng, Dar-Ren Chen, Yi-Chia Wu, Ming-Feng Hou, Shyng-Shiou F. Yuan, Cancers, 12, 29 (1), 2019
Adipose-derived stem cells (ADSCs) have been implicated in tumor growth and metastasis in breast cancer. ADSCs exhibit tumor tropism, and are of increasing clinical relevance due to the autologous fat grafting for breast reconstruction. Although we have previously shown that a high level of the adipocytokine visfatin in human breast cancer tissues correlated with tumor progression mediated by cAbl and STAT3, the effects of visfatin in the tumor microenvironment are unclear. To understand how visfatin modulates breast cancer within the tumor-stromal environment, we examined determinants of breast cancer progression using a visfatin-primed ADSCs-tumor co-culture model. ADSCs were isolated from tumor-free adipose tissue adjacent to breast tumors. ADSCs were treated with or without visfatin for 48 h and then collected for co-culture with breast cancer cell line MDA-MB-231 for 72 h in a transwell system. We found that the MDA-MB-231 cells co-cultured with visfatin-treated ADSCs (vADSCs) had higher levels of cell viability, anchorage independent growth, migration, invasion, and tumorsphere formation than that co-cultured with untreated ADSCs (uADSCs). Growth differentiation factor 15 (GDF15) upregulation was found in the co-culture conditioned medium, with GDF15 neutralizing antibody blocking the promoting effect on MDA-MB-231 in co-culture. In addition, a GDF15-induced AKT pathway was found in MDA-MB-231 and treatment with PI3K/AKT inhibitor also reversed the promoting effect. In an orthotopic xenograft mouse model, MDA-MB-231 co-injected with vADSCs formed a larger tumor mass than with uADSCs. Positive correlations were noted between visfatin, GDF15, and phosphor-AKT expressions in human breast cancer specimens. In conclusion, visfatin activated GDF15-AKT pathway mediated via ADSCs to facilitate breast cancer progression.
Marta Mascaraque, Pablo Delgado-Wicke, Cristina Nuevo-Tapioles, Tamara Gracia-Cazaña, Edgar Abarca-Lachen, Salvador González, José M. Cuezva, Yolanda Gilaberte, Ángeles Juarranz, Cancers, 12, 668 (3), 2020
Photodynamic Therapy (PDT) with methyl-aminolevulinate (MAL-PDT) is being used for the treatment of Basal Cell Carcinoma (BCC), although resistant cells may appear. Normal differentiated cells depend primarily on mitochondrial oxidative phosphorylation (OXPHOS) to generate energy, but cancer cells switch this metabolism to aerobic glycolysis (Warburg effect), influencing the response to therapies. We have analyzed the expression of metabolic markers (β-F1-ATPase/GAPDH (glyceraldehyde-3-phosphate dehydrogenase) ratio, pyruvate kinase M2 (PKM2), oxygen consume ratio, and lactate extracellular production) in the resistance to PDT of mouse BCC cell lines (named ASZ and CSZ, heterozygous for ptch1). We have also evaluated the ability of metformin (Metf), an antidiabetic type II compound that acts through inhibition of the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway to sensitize resistant cells to PDT. The results obtained indicated that resistant cells showed an aerobic glycolysis metabolism. The treatment with Metf induced arrest in the G0/G1 phase and a reduction in the lactate extracellular production in all cell lines. The addition of Metf to MAL-PDT improved the cytotoxic effect on parental and resistant cells, which was not dependent on the PS protoporphyrin IX (PpIX) production. After Metf + MAL-PDT treatment, activation of pAMPK was detected, suppressing the mTOR pathway in most of the cells. Enhanced PDT-response with Metf was also observed in ASZ tumors. In conclusion, Metf increased the response to MAL-PDT in murine BCC cells resistant to PDT with aerobic glycolysis.
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