Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heparin-binding EGF-like growth factor (HB-EGF) and amphiregulin (AREG) are the members of EGF family that bind to common EGF receptor (EGFR) in the epidermis. However, the role of these two growth factors in epidermal hyperplasia of psoriasis has not been established. On the other hand, CD4+ T cells are responsible for the development of the psoriatic plaques. However, inflammatory cytokines, such as TNFalpha, IL-1beta and IFNgamma, inhibit the growth of human keratinocytes in vitro. The expression of HB-EGF, AREG and EGFR proteins in normal (n = 22) and psoriatic (n = 34) skin tissues was examined by immunohistochemistry. Then, the effects of HB-EGF and AREG on the growth of cultured adult normal human epidermal keratinocytes (NHEK-AD) with or without TH1 cytokines, such as TNFalpha, IL-1beta and IFNgamma, were examined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay, and the effects of these cytokines on the expression of EGFR mRNA in NHEK-AD were examined by real-time reverse transcriptase-polymerase chain reaction. The expression of HB-EGF and AREG in the epidermis was not specific to psoriatic plaques, but the distribution of positive cells throughout the epidermis was different between normal skins and psoriatic plaques. On the other hand, in the dermis and the papillary dermis, most of vascular endothelial cells and infiltrating mononuclear cells expressed both HB-EGF and AREG in normal skins and psoriatic plaques, and these positive cells were more frequent in psoriasis compared to normal skin. In the in vitro growth assay, HB-EGF, not AREG, stimulated the proliferation of NHEK-AD at the optimal concentration of 1 ng/ml. Furthermore, HB-EGF compensated the growth-suppressing effects of TNFalpha, IL-1beta and IFNgamma on NHEK-AD, and TNFalpha promoted the growth of NHEK-AD at the concentration of 2 and 20 U/ml in combination with HB-EGF and, in lesser extent, with AREG. However, TNFalpha did not affect the expression of EGFR mRNA in NHEK-AD. Growth factors and inflammatory cytokines produced in the dermis would be important for the epidermal proliferation in psoriatic plaques and TNFalpha may play a key role in cooperation with HB-EGF and AREG in the proliferation of epidermal keratinocytes at the psoriatic skin lesions.
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PMID:The role of heparin-binding EGF-like growth factor and amphiregulin in the epidermal proliferation of psoriasis in cooperation with TNFalpha. 1796 Apr

In the present study, the toxicity of arsenic trioxide and lead acetate was assessed in adult hepatic stem cells induced in the 2-acetyl-aminofluorene/partial hepatectomy rat model. Isolated oval cells were incubated separately for 6 h with 40 muM each of arsenic trioxide and lead acetate. 3-(4,5-Dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromide assay denoted significant time-dependent cell death in arsenic and lead treated oval cells. The degree of stress imposed by these metals was evidenced by induction of heat shock protein (HSP) 70 and HSP 90. Arsenic and lead were found to trigger apoptosis as revealed by DNA ladder formation, Western blots of apoptotic factors, and reverse transcriptase polymerase chain reaction analyses of bax and bcl-2. Results clearly indicate that both arsenic and lead induced apoptosis is caspase-mediated and accompanied by extracellular signal-regulated kinase (ERK) dephosphorylation. Full-length BH3-interacting-domain death agonist expression in presence of caspase 3 inhibitor unravels a direct involvement of caspase in As and Pb induced apoptosis. Expression patterns of apoptosis inducing factor, B cell lymphoma-2 (Bcl-2) antagonist of cell death, Bcl-2-associated X protein, and Bcl2 also signify mitochondrial regulation of apoptosis effected by lead and arsenic. It is concluded that stimulation of caspase cascade and simultaneous ERK dephosphorylation are the most significant operative pathways directly associated with apoptotic signals triggered by arsenic and lead in the oval cells.
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PMID:Arsenic trioxide and lead acetate induce apoptosis in adult rat hepatic stem cells. 1861 74

In recent years, natural dietary agents have drawn a great deal of attention owing to their demonstrated ability to suppress cancer. We aimed to investigate the in-vitro gastric cancer preventive activity of a methanol extract obtained from table olives of Greek origin. Tested were AGS cell proliferation, induction of apoptosis and inhibition of inflammation. AGS stomach cancer cells were cultured at a density of 10 cells/ml. Methanol extract of olive was added to cultures at concentrations of 2.0, 1.6, 1.0, and 0.4 microg phenols/ml. Effect on cellular viability was evaluated via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and percentages of early and late apoptotic cells were assayed by annexin V-FITC staining on a FACS scan. Interleukin-8 (IL-8) and intercellular adhesion molecule (ICAM)-1 mRNA and protein production were measured by applying reverse transcriptase-PCR and enzyme-linked immunosorbent assay. Olive extract significantly suppressed cell proliferation at 2.0, 1.6, and 1.0 microg phenols/ml. Flow cytometric analysis of Annexin-V labeled cells indicated that 2.0 microg phenols/ml significantly induced apoptosis. Similarly, at 2.0, 1.6, and 1.0 microg phenols/ml a significant decrease of ICAM-1 and IL-8 protein levels was observed. ICAM-1, as well as IL-8, mRNA expression were decreased in the presence of 2.0 microg phenols/ml. Results indicate that the methanol extract from olives, rich in phenolic compounds, exhibits gastric cancer preventive efficacy by limiting cell proliferation, inducing cell death and suppressing inflammation in AGS cells.
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PMID:In-vitro gastric cancer prevention by a polyphenol-rich extract from olives through induction of apoptosis. 1907 62

We previously established H-1R cells, a cisplatin (CDDP)-resistant cell line, from H-1 cells, a CDDP-sensitive oral carcinoma cell line. The aim of this study was to identify the molecular mechanism of cross-resistance to antitumor drugs containing a platinum agent in H-1R cells. The 3-(3,4-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay and clonogenecity assay indicated that H-1R cells showed strong cross-resistance to carboplatin, nedaplatin and oxaliplatin. The expression status of the copper transporter and organic cation transporters was confirmed by real-time quantitative reverse transcriptase-polymerase chain reaction. The transporters ATP7A, ATP7B, hCtr1, hOCT1 and hOCT2 were up-regulated, whereas hOCT3 was down-regulated. The cellular glutathione level was elevated 2-fold in H-1R cells compared with H-1 cells. Our results suggested that H-1 and H-1R cells may be useful in searching for candidate genes responsible for cross-resistance to platinum derivatives and for further studies to understand the mechanism of platinum resistance.
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PMID:Cross-resistance of platinum derivatives in H-1R, a cisplatin-resistant cell line. 1914 21

Drug resistance is the major setback of acute myeloid leukemia (AML) therapy. Notch proteins have demonstrated functional regulation in cell proliferation, differentiation, and apoptosis and thus may affect drug resistance. Our study aimed to identify the Notch-related gene profile in drug-resistant AML cells and provide potential strategies for resistant AML therapy. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was conducted to detect the cytotoxicity of adriamycin toward K562 and drug-resistant K562/A02. Intracellular mean fluorescence intensity was monitored to reflect the intake of adriamycin by confocal microscopy. cDNA microarray was used to test the expression of 113 Notch signaling pathway-related genes in K562/A02 and K562. Real-time reverse transcriptase polymerase chain reaction (RT-PCR) and western blot were used to validate the results from microarray. K562/A02 cells showed a 65-fold higher IC(50) to adriamycin and less intracellular accumulation of adriamycin than K562. cDNA microarray showed marked increases in binding of collagen and cell proliferation-related genes (CD44, DLL3, IL17B, NUMB, and NUMBL) and decreases in signal transduction and transcription factor activity related genes (FZD9, GBP2, GLI1, GLI2, IFNG, KRT5, Notch2, and Notch3). The change of gene expression was further validated by real-time RT-PCR and western blot. Notch signaling pathway-related genes may contribute to the drug resistance of AML.
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PMID:Expression profile of Notch-related genes in multidrug resistant K562/A02 cells compared with parental K562 cells. 1930 34

Bone cell (MG63) biocompatibility and bone marker expression were compared after calcium and silicate base cement (CS) and mineral trioxide aggregate (MTA) treatment. X-ray diffraction was used to identify material surface structure, and tetrazolium bromide colorimetric assay was used to evaluate the cell viability. The relative mitogen activation protein kinase expression was compared with Western blot, and bone marker expression was evaluated with reverse transcriptase polymerization chain reaction. The results showed that CS and MTA are similar chemical structures and biocompatible with MG63 cells. CS and MTA cements showed good MG63 cell proliferation by high phosphor extracellular signal-regulated kinase expression levels. CS and MTA cements showed the evident type I collagen, osteocalcin, alkaline phosphatase, bone sialoprotein, and osteopontin expression. Both MTA and CS cements are biocompatible and appear to have osetoconduction effects on bone cells.
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PMID:Comparison of calcium and silicate cement and mineral trioxide aggregate biologic effects and bone markers expression in MG63 cells. 1941 82

This study was to investigate whether ascorbic acid (AA) at pharmacologic concentration became prooxidant and had the potential to influence the expressions of angiogenic and angiostatic chemokine genes in hepatocellular carcinoma (HCC) cell lines. Influence of low (1 mM) and high (30 mM) pharmacologic concentrations of AA on two HCC cell lines (cell line A, HCC24/KMUH; cell line B, HCC38/KMUH) were studied by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Three angiogenic genes (CCL2, CXCL6, IL8), one angiostatic gene (CXCL10) and two genes related to oxidative stress (SOD2, VNN3) were selected for quantitative RT-PCR study. Both low and high pharmacologic concentrations of AA up-regulated CCL2, CXCL6, IL8, SOD2 and VNN3 genes in cell line A, but down-regulated CCL2 and IL8 genes in cell line B. CXCL6 gene in cell line B was down-regulated by high pharmacologic concentration of AA. CXCL10 gene was up-regulated by low pharmacologic concentration of AA, but was down-regulated by high pharmacologic concentration of AA in both cell lines. Low pharmacologic concentration of AA up-regulated VNN3 gene and high pharmacologic concentration of AA up-regulated SOD2 gene in cell line B. These results indicate that pharmacologic concentration of AA becomes prooxidant to HCC cells and has diverse influence on differential expressions of angiogenic chemokine genes in different HCC cell lines. Differential expressions of CXCL10 gene are determined by the concentrations of AA used. Clinical application of AA in patients with HCC should consider these effects.
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PMID:Pharmacologic concentrations of ascorbic acid cause diverse influence on differential expressions of angiogenic chemokine genes in different hepatocellular carcinoma cell lines. 1993 82

The hepatotoxicity induced by valproic acid (VPA) has been described in many clinical studies and the related mechanism has been partly elucidated. The objective of this study is to investigate the hepatotoxicity and its underlying mechanism of valproic acid on human hepatoma carcinoma cell line HepG2. The cell viability was evaluated by 3-(4,5-dimethyltyiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) in the medium were detected using spectrophotometry. The gene expressions of cytochrome P450 1 A1 (CYP1A1), ATP-binding cassette transporter G1 (ABCG1) and carnitine palmitoyltransferase 1 (CPT1A), related to lipid transport and fatty acid metabolism, were measured by quantitative real-time reverse transcriptase-PCR. Treatment with valproate sodium obviously decreased the viability of HepG2 cells, accompanied by the increased leakages of ALT, AST and LDH in a dose-dependent manner. Furthermore, the gene expressions of CYP1A1, ABCG1 and CPT1A were almost up-regulated in the treated groups. In conclusion, these data suggest that VPA-induced hepatotoxicity was critically enhanced with the elevation of valproate sodium, which may be correlated with up-regulated gene expressions of CYP1A1, ABCG1 and CPT1A.
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PMID:Participation of lipid transport and fatty acid metabolism in valproate sodium-induced hepatotoxicity in HepG2 cells. 2037 Dec 85

This study was purposed to investigate the expression of RPL36A (ribosomal protein 36a) in the newly diagnosed acute myeloid leukemia (AML) cells and its mechanism at the molecular level. The RPL36A mRNA expression in the newly diagnosed AML cells, U937 cells and normal MNCs was determined by RT-PCR. Small interfering RNA (siRNA) targeting to RPL36A was transfected into U937 cells by Lipofectamine 2000 system. Proliferation, cell cycle, apoptosis of U937 were observed through MTT assay, flow cytometry, acridine orange/ethidium bromide (AO/EB) double staining, TUNEL and Annexin V/FITC respectively. RPL36A mRNA and protein expression levels were detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analysis respectively. The results showed that RPL36A expression in the newly diagnosed AML cells and U937 cells was significantly upregulated. The average OD value of U937 cells transfected with RPL36A siRNA was significantly lower as compared with 3 control groups. The cell percentage in G2-and S-phase increased, which indicated the inhibition effect of RPL36A siRNA on cell proliferation. Remarkable cell apoptosis in U937 cells treated with RPL36A siRNA was observed by AO/EB, TUNEL analysis and Annexin V/FITC assay; RPL36A mRNA and protein expression level of U937 cells treated with siRNA were significantly declined in a time-dependent manner (r=0.9813 and 0.9537). It is concluded that the RPL36A expression in the AML cells is significantly enhanced and the RPL36A gene may be involved in regulation of cell cycle and cell apoptosis of AML, which promotes proliferation of AML cells and inhibits apoptosis of cells.
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PMID:[Proliferation promotion and apoptotic inhibition effects of ribosomal protein RPL36A small interference RNA on U937 cells]. 2041 65

The RegIV gene is differentially expressed in cancer and noncancerous cells. In this study, we investigated the role of RegIV and its CRD domain in the invasion and migration of human colorectal carcinoma LoVo cells. Recombinant plasmids, pcDNA3.1-RegIV and pcDNA3.1-RegIV CRD, were constructed and transfected into LoVo cells. The in vivo RegIV and RegIV CRD mRNA and protein levels were then analyzed by reverse transcriptase-polymerase chain reaction and immunocytochemistry, respectively. Cell proliferation was measured by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and flat plate colony-forming assays, and apoptosis was measured by flow cytometry. Cell migration and invasion were assessed with a Transwell chamber. A high level of RegIV and RegIV carbohydrate-recognition domain (CRD) expression was demonstrated in RegIV and RegIV CRD-transfected cells. There were no differences in cell proliferation, colony formation, and apoptosis between the LoVo/RegIV and untreated LoVo cells (P > 0.05). However, the LoVo/RegIV cells, but not LoVo/RegIV CRD cells, displayed greater migration and invasion abilities compared to the empty vector and untreated LoVo cells. The migrated cell numbers of the LoVo/RegIV, LoVo/RegIV CRD, LoVo/empty vector, and control LoVo groups were 247.00 +/- 10.61, 146.27 +/- 6.81, 151.16 +/- 7.18, and 149.65 +/- 6.53 cells per field, respectively (P < 0.05). The invasion cell numbers of the four groups were 57.00 +/- 3.00, 31.53 +/- 2.72, 30.3 +/- 2.07, and 32.16 +/- 2.30 cells per field, respectively. RegIV enhances LoVo cell migration and invasion, and its CRD domain is critical for these effects.
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PMID:RegIV potentiates colorectal carcinoma cell migration and invasion via its CRD domain. 2041 67


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