Activated carbon (AC)/CoFe
2
O
4
nanocomposites, MAC-1 and MAC-2, were prepared by a simple pyrolytic method using a mixture of iron(III)/cobalt(II) benzoates and iron(III)/cobalt(II) oxalates, ...respectively, and were used as efficient adsorbents for the removal of amoxicillin (AMX) and paracetamol (PCT) of aqueous effluents. The synthesized nanocomposites were characterized by X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR), vibrating sample magnetometry (VSM), scanning electron microscopy (SEM), energy dispersive X-ray spectroscopy (EDX) and transmission electron microscopy (TEM). The sizes of cobalt ferrite nanoparticles formed from benzoates of iron(III)/cobalt(II) and oxalates of iron(III)/cobalt(II) precursors were in the ranges of 5–80 and 6–27 nm, respectively. The saturation magnetization (
M
s
), remanence (
M
r
) and coercivity (
H
c
) of the MAC-2 nanocomposites were found to be 3.07 emu g
−1
, 1.36 emu g
−1
and 762.49 Oe; for MAC-1, they were 0.2989 emu g
−1
, 0.0466 emu g
−1
and 456.82 Oe. The adsorption kinetics and isotherm studies were investigated, and the results showed that the as-prepared nanocomposites MAC-1 and MAC-2 could be utilized as an efficient, magnetically separable adsorbent for environmental cleanup. The maximum sorption capacities obtained were 280.9 and 444.2 mg g
−1
of AMX for MAC-1 and MAC-2, respectively, and 215.1 and 399.9 mg g
−1
of PCT using MAC-1 and MAC-2, respectively. Both adsorbents were successfully used for simulated hospital effluents, removing at least 93.00 and 96.77% for MAC-1 and MAC-2, respectively, of a mixture of nine pharmaceuticals with high concentrations of sugars, organic components and saline concentrations.
SOCS1 in cancer: An oncogene and a tumor suppressor Beaurivage, Claudia; Champagne, Audrey; Tobelaim, William S. ...
Cytokine (Philadelphia, Pa.),
June 2016, 2016-Jun, 2016-06-00, 20160601, Volume:
82
Journal Article
Peer reviewed
The Suppressor Of Cytokine Signaling 1 (SOCS1) has been extensively investigated in immune cells where it works as a potent inhibitor of inflammation by negative feedback regulation of the ...cytokine-activated JAK–STAT signaling pathways. SOCS1 is also recognized as a tumor suppressor in numerous cancers and its critical functional relevance in non-immune cells, including epithelial cells, has just begun to emerge. Most notably, conflicting results from clinical and experimental studies suggest that SOCS1 may function as either a tumor suppressor or a tumor promoter, in a cell context-dependent manner. Here, we present an overview of the mechanisms underlying SOCS1 function as a tumor suppressor and discuss the emerging evidences of SOCS1 activity as an oncogene.
AIM To investigate the role of suppressor of cytokine signaling 1(SOCS1)in regulating MET-mediated invasive potential of hepatocellular carcinoma(HCC)cells.METHODSStable derivatives of ...mouse(Hepa1-6)and human(hep3B,Hep G2)HCC cell lines expressing SOCS1or control vector were evaluated for their ability to migrate towards hepatocyte growth factor(HGF)in the transwell migration assay,invade extracellular matrix in response to HGF stimulation in a 3-D invasion assay by confocal microscopy,and to undergo anchorageindependent proliferation in semisolid agar.Following intravenous and intrasplenic inoculation into NOD.scid.gamma mice,the ability of Hepa cells to form othotopic tumors was evaluated.Following HGF stimulation of Hepa and Hep3B cells,expression of proteins implicated in epithelial-to-mesenchymal transition was evaluated by western blot and qR T-PCR.RESULTS SOCS1 expression in mouse and human HCC cells inhibited HGF-induced migration through matrigel.In the 3-D invasion assay,HGF stimulation induced invasion of HCC cells across type-Ⅰcollagen matrix,and SOCS1expression significantly reduced the depth of invasion.SOCS1 expression also reduced the number and size of colonies formed by anchorage-independent growth in semisolid agar.Following intravenous inoculation,control Hepa cell formed large tumor nodules that obliterated the liver whereas the SOCS1-expressing Hepa cells formed significantly smaller nodules.Tumors formed by SOCS1-expressing cells showed reduced phosphorylation of STAT3 and ERK that was accompanied by reduced levels of MET protein expression.HGF stimulated Hepa cells expressing SOCS1 showed increased expression of E-cadherin and decreased expression of EGR1,SNAI1and ZEB1.Comparable results were obtained with Hep3B cells.SOCS1 expressing HCC cells also showed reduced levels of EGR1 and SNAI1 transcripts.CONCLUSION Our findings indicate that loss of SOCS1-dependent control over epithelial-to-mesenchymal transition may contribute to MET-mediated migration,invasion and metastatic growth of HCC.
Hypoxia is a common characteristic of advanced solid tumors and a potent driver of tumor invasion and metastasis. Recent evidence suggests the involvement of autotaxin (ATX) and lysophosphatidic acid ...receptors (LPARs) in cancer cell invasion promoted by the hypoxic tumor microenvironment; however, the transcriptional and/or spatiotemporal control of this process remain unexplored. Herein, we investigated whether hypoxia promotes cell invasion by affecting the main enzymes involved in its production (ATX) and degradation (lipid phosphate phosphatases, LPP1 and LPP3). We report that hypoxia not only modulates the expression levels of lysophosphatidic acid (LPA) regulatory enzymes but also induces their significant spatial segregation in a variety of cancers. While LPP3 expression was downregulated by hypoxia, ATX and LPP1 were asymmetrically redistributed to the leading edge and to the trailing edge, respectively. This was associated with the opposing roles of ATX and LPPs in cell invasion. The regulated expression and compartmentalization of these enzymes of opposing function can provide an effective way to control the generation of an LPA gradient that drives cellular invasion and migration in the hypoxic zones of tumors.
Sludge based activated carbons (ACs) were used to remove selected pharmaceuticals such as diclofenac (DCF) and nimesulide (NM) from aqueous solutions. The powered sewage sludge was mixed with ...different proportions of ZnCl
2
. The mixture was pyrolyzed in a conventional oven using three different temperatures under inert atmosphere. Afterwards, in order to increase the specific surface area and uptake capacity the carbonized materials were acidified with 6mol L
−1
HCl under reflux at 80 °C for 3 hours. The characterization of ACs was achieved by scanning electron microscopy, FTIR, TGA, hydrophobicity index by water, n-heptane vapor adsorption and nitrogen adsorption/desorption curves. The specific surface area (S
BET
) of adsorbents varied between 21.2 and 679.3m
2
g
−1
. According to the water and n-heptane analysis data all ACs had hydrophobic surface. Experimental variables such as pH, mass of adsorbent and temperature on the adsorption capacities were studied. The optimum pH, mass of adsorbent and temperature for adsorption of DCF and NM onto ACs were found to be 7.0 (DCF) and 10.0 (NM), 30mg and 25 °C, respectively. The kinetic adsorption was investigated using general-order, pseudo-first order and pseudo-second order kinetic models, while the general-order model described the adsorption process most suitably. The maximum amounts of DCF and NM adsorbed were 156.7 and 66.4mg g
−1
for sample 1(500-15-0.5), respectively.
Suppressor of cytokine signaling 1 (SOCS1) is considered a tumor suppressor due to frequent epigenetic and micro-RNA-mediated repression of its gene expression in diverse cancers. In prostate cancer ...(PCa), elevated expression of miR-30d that targets SOCS1 mRNA is associated with increased risk of disease recurrence. SOCS1 can mediate its tumor suppressor functions by diverse mechanisms such as inhibiting the JAK-STAT signaling pathway, promoting the tumor suppressor functions of p53, attenuating MET receptor tyrosine kinase signaling and blocking the oncogenic potential of the cell cycle inhibitor p21
(p21). Here, we studied the expression of SOCS1 and the downstream targets of its putative tumor suppressor functions (p53, MET and p21) in human PCa specimens to evaluate their significance as markers of disease prognosis.
Tissue microarrays were constructed of 78 archived prostatectomy specimens that were grouped according to the recommendations of the International Society of Urological Pathology (ISUP) based on the Gleason patterns. SOCS1, p53, MET and p21 protein expression were evaluated by immunohistochemical staining alongside the common prostate cancer-related markers Ki67, prostein and androgen receptor. Statistical correlations between the staining intensities of these markers and ISUP grade groups, local invasion or lymph node metastasis were evaluated.
SOCS1 showed diffuse staining in the prostatic epithelium. SOCS1 staining intensity correlated inversely with the ISUP grade groups (ρ = -0.4687, p <0.0001) and Ki67 (ρ = -0.2444, p = 0.031), and positively with prostein (ρ = 0.3511, p = 0.0016). Changes in SOCS1 levels did not significantly associate with those of p53, MET or p21. However, p21 positively correlated with androgen receptor expression (ρ = -0.1388, p = 0.0003). A subset of patients with regional lymph node metastasis, although small in number, showed reduced SOCS1 expression and increased expression of MET and p21.
Our findings suggest that evaluating SOCS1 and p21 protein expression in prostatectomy specimens may have a prognostic value in identifying the aggressive disease. Hence, prospective studies with larger numbers of metastatic PCa specimens incorporating clinical correlates such as disease-free and overall survival are warranted.
The PTEN phosphatase acts on phosphatidylinositol 3,4,5-triphosphates resulting from phosphatidylinositol 3-kinase (PI3K) activation. PTEN expression has been shown to be decreased in colorectal ...cancer. Little is known however as to the specific cellular role of PTEN in human intestinal epithelial cells. The aim of this study was to investigate the role of PTEN in human colorectal cancer cells.
Caco-2/15, HCT116 and CT26 cells were infected with recombinant lentiviruses expressing a shRNA specifically designed to knock-down PTEN. The impact of PTEN downregulation was analyzed on cell polarization and differentiation, intercellular junction integrity (expression of cell-cell adhesion proteins, barrier function), migration (wound assay), invasion (matrigel-coated transwells) and on tumor and metastasis formation in mice. Electron microscopy analysis showed that lentiviral infection of PTEN shRNA significantly inhibited Caco-2/15 cell polarization, functional differentiation and brush border development. A strong reduction in claudin 1, 3, 4 and 8 was also observed as well as a decrease in transepithelial resistance. Loss of PTEN expression increased the spreading, migration and invasion capacities of colorectal cancer cells in vitro. PTEN downregulation also increased tumor size following subcutaneous injection of colorectal cancer cells in nude mice. Finally, loss of PTEN expression in HCT116 and CT26, but not in Caco-2/15, led to an increase in their metastatic potential following tail-vein injections in mice.
Altogether, these results indicate that PTEN controls cellular polarity, establishment of cell-cell junctions, paracellular permeability, migration and tumorigenic/metastatic potential of human colorectal cancer cells.
New carbon composite materials were prepared by pyrolysis of mixture of coffee wastes and red mud at 700 °C with the inorganic: organic ratios of 1.9 (CC-1.9) and 2.2 (CC-2.2). These adsorbents were ...used to remove reactive orange 16 (RO-16) and reactive red 120 (RR-120) textile dyes from aqueous solution. The CC-1.9 and CC-2.2 materials were characterized using Fourier transform infrared spectroscopy, Nitrogen adsorption/desorption curves, scanning electron Microscopy and X-ray diffraction. The kinetic of adsorption data was fitted by general order kinetic model. A three-parameter isotherm model, Liu isotherm model, gave the best fit of the equilibrium data (298 to 323 K). The maximum amounts of dyes removed at 323 K were 144.8 (CC-1.9) and 139.5 mg g
−1
(CC-2.2) for RO-16 dye and 95.76 (CC-1.9) and 93.80 mg g
−1
(CC-2.2) for RR-120 dye. Two simulated dyehouse effluents were used to investigate the application of the adsorbents for effluent treatment.
PDF
