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#29043702   2017/10/18 Save this To Up

N-Acetylcysteine Compared to Metformin, Improves The Expression Profile of Growth Differentiation Factor-9 and Receptor Tyrosine Kinase c-Kit in The Oocytes of Patients with Polycystic Ovarian Syndrome.

Paracrine disruption of growth factors in women with polycystic ovarian syndrome (PCOS) results in production of low quality oocyte, especially following ovulation induction. The aim of this study was to investigate the effects of metformin (MET), N-acetylcysteine (NAC) and their combination on the hormonal levels and expression profile of GDF-9, BMP-15 and c-kit, as hallmarks of oocyte quality, in PCOS patients.

2082 related Products with: N-Acetylcysteine Compared to Metformin, Improves The Expression Profile of Growth Differentiation Factor-9 and Receptor Tyrosine Kinase c-Kit in The Oocytes of Patients with Polycystic Ovarian Syndrome.

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#29041983   2017/10/18 Save this To Up

PAK5-mediated phosphorylation and nuclear translocation of NF-κB-p65 promotes breast cancer cell proliferation in vitro and in vivo.

Abnormal proliferation is significantly associated with the promotion of malignant tumor. Growing evidence suggest that the signal pathways of p21(cdc42/rac1)-activated kinase 5 (PAK5) have been found in various tumor progression, however, the role of PAK5 in breast cancer remains largely unclear.

1134 related Products with: PAK5-mediated phosphorylation and nuclear translocation of NF-κB-p65 promotes breast cancer cell proliferation in vitro and in vivo.

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#29039492   2017/10/17 Save this To Up

Black rice-derived anthocyanins inhibit HER-2-positive breast cancer epithelial-mesenchymal transition-mediated metastasis in vitro by suppressing FAK signaling.

This study aimed to investigate the role of focal adhesion kinase (FAK) signaling in the inhibitory effects of black rice anthocyanins (BRACs) on human epidermal growth factor receptor-2 (HER-2)-positive human breast cancer cell metastasis, using the MCF-10A, MCF-7 and MDA-MB-453 cells. BRACs exerted an anti-metastatic effect on the HER-2-positive breast cancer cells. The effects of BRACs on the proliferation of the MDA-MB-453 cells were examined by cell counting kit-8 assay. A wound-healing assay was used to examine the effects of BRACs on the migration of the breast cancer cells. BRACs interrupted migration and invasion. BRACs decreased the migration distance of the HER-2-positive human breast cancer cells, MDA-MB-453, by 37% compared with the cells in the untreated group. They also reduced the number of invading MDA-MB-453 cells by 68%. In addition, BRACs exerted an inhibitory effect on epithelial-mesenchymal transition. Western blot analysis revealed that BRACs decreased the phosphorylation of FAK, cSrc and p130Cas. The FAK inhibitor, Y15, was also used to further evaluate the role of FAK signaling in the anti-metastatic effects of BRACs on MDA-MB-453 cells. The results of western blot analysis revealed that BRACs increased the expression of the epithelial marker, E-cadherin, and decreased the expression of the mesenchymal markers, fibronectin and vimentin, in the MDA-MB‑453 cells. In addition, BRACs decreased the interaction between HER-2 and FAK, FAK and cSrc, cSrc and p130Cas, and between FAK and p130Cas. These results suggest that BRACs suppress the metastasis of HER-2-positive breast cancer in vitro, and that the cSrc/FAK/p130Cas pathway plays a vital role in this inhibitory effect.

1626 related Products with: Black rice-derived anthocyanins inhibit HER-2-positive breast cancer epithelial-mesenchymal transition-mediated metastasis in vitro by suppressing FAK signaling.

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#29035884   2017/10/16 Save this To Up

Protective Effects of Pretreatment with Quercetin Against Lipopolysaccharide-Induced Apoptosis and the Inhibition of Osteoblast Differentiation via the MAPK and Wnt/β-Catenin Pathways in MC3T3-E1 Cells.

Quercetin, a flavonoid found in onions and other vegetables, has potential inhibitory effects on bone resorption in vivo and in vitro. In our previous study, we found that quercetin treatment reversed lipopolysaccharide (LPS)-induced inhibition of osteoblast differentiation through the mitogen-activated protein kinase (MAPK) pathway in MC3T3-E1 cells. In this study, we investigated the underlying mechanisms of pretreatment with quercetin on apoptosis and the inhibition of osteoblast differentiation in MC3T3-E1 cells induced by LPS.

1396 related Products with: Protective Effects of Pretreatment with Quercetin Against Lipopolysaccharide-Induced Apoptosis and the Inhibition of Osteoblast Differentiation via the MAPK and Wnt/β-Catenin Pathways in MC3T3-E1 Cells.

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#29035863   2017/10/16 Save this To Up

Sero-detection of Toxocara canis infection in human with T.canis recombinant arginine kinase, cathepsin L-1 and TES-26 antigens.

Three recombinant antigens viz. arginine kinase, cathepsin L-1 and TES-26 of Toxocara canis were expressed in Escherichia coli and evaluated for their potential in the detection of T. canis larval infection in human in immunoglobulin G-enzyme linked immunosorbent assay (IgG-ELISA). Results of the IgG-ELISA with the above recombinant antigens were confirmed with commercially available IgG detection kit for T. canis infection used as a standard test. All three recombinant antigens were 100% sensitive in the detection of positive cases (n = 6) of T. canis infection in human and were screened for their cross-reactivity in human patients with history of Toxoplasma gondii, Plasmodium vivax, Entamoeba histolytica, hydatid and hookworm infections. The recombinant TES-26 antigen showed higher specificity and cross-reacted with T. gondii infection sera only. However, arginine kinase and cathepsin L-1 recombinant antigens showed cross-reactions with sera of patients infected with T. gondii, P. vivax and E. histolytica but not with the patient sera infected with hydatid and hookworm. These results show that recombinant TES-26 is a potential diagnostic candidate antigen for human toxocarosis caused by migrating T. canis larvae.

1230 related Products with: Sero-detection of Toxocara canis infection in human with T.canis recombinant arginine kinase, cathepsin L-1 and TES-26 antigens.

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#28990044   2017/10/09 Save this To Up

MicroRNA‑320 targets mitogen‑activated protein kinase 1 to inhibit cell proliferation and invasion in epithelial ovarian cancer.

Ovarian cancer is the second most frequently occurring cancer and the most fatal gynecological malignancy of all gynecological cancers worldwide. MicroRNAs (miR) have been reported to be downregulated or upregulated in a variety of human malignancies, and involved in the formation and progression of the majority of human cancers, including epithelial ovarian cancer (EOC). miR‑320 has been identified as a tumor suppressor in multiple human cancers. However, the expression levels, biological role and underlying mechanisms of miR‑320 in EOC remain to be elucidated. In the present study, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to detect miR‑320 expression in EOC tissues and cell lines. Following transfection with miR‑320 mimics, Cell Counting Kit 8 and cell invasion assays were utilized to investigate the effects of miR‑320 on EOC cell proliferation and invasion. Bioinformatic analysis, luciferase reporter assay, RT‑qPCR and western blotting were used to explore the underlying mechanism of how miR‑320 affects cell proliferation and invasion in EOC. Mitogen‑activated protein kinase (MAPK) 1 expression and its association with the miR‑320 expression level was examined in EOC tissues. The role of MAPK1 in EOC cells was additionally evaluated by using a loss‑of‑function assay. The results demonstrated that miR‑320 was markedly downregulated in EOC tissues and cell lines. A decreased miR‑320 expression was significantly correlated with the Federation of Gynecology and Obstetrics stage and lymph node metastasis of EOC patients. Additionally, reintroduction of miR‑320 expression suppressed cell proliferation and invasion in EOC. Furthermore, it was verified that MAPK1 is a direct target gene of miR‑320 in EOC. MAPK1 expression was markedly upregulated in EOC tissues and inversely correlated with miR‑320 expression. Furthermore, silencing of MAPK1 by RNA interference inhibited cell proliferation and invasion of EOC cells. Overall, the present study demonstrated that miR‑320 may act as a useful diagnostic and therapeutic target in the treatment of EOC.

1950 related Products with: MicroRNA‑320 targets mitogen‑activated protein kinase 1 to inhibit cell proliferation and invasion in epithelial ovarian cancer.

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#28990042   2017/10/09 Save this To Up

Hydroxytyrosol contributes to cell proliferation and inhibits apoptosis in pulsed electromagnetic fields treated human umbilical vein endothelial cells in vitro.

A variety of pulsed electromagnetic fields (PEMFs) have been experimentally and clinically used in an effort to promote wound healing, although the mechanisms involved remain unknown. The aim of the present study was to investigate the action of a novel protocol of co‑treatment with PEMFs and hydroxytyrosol (HTY) on the proliferation and differentiation potential of human umbilical vein endothelial cells (HUVECs). The HUVECs were assigned randomly into three groups: Control, PEMF‑treated and PEMF + HT‑treated. The intensity of the electromagnetic field used in this protocol was 2.25 mT, the frequency of the bursts was 50 Hz and the application time was 15 min. A Cell Counting kit‑8 (CCK‑8) assay was used to assess cell proliferation, and cell apoptosis was analyzed by TUNEL apoptosis assay kit and calcein‑acetoxymethyl/propidium iodide dual‑staining assay. In addition, protein and mRNA expression levels of protein kinase B (Akt), mechanistic target of rapamycin (mTOR), transforming growth factor (TGF)‑β1 and p53 were determined by western blotting and reverse transcription‑quantitative polymerase chain reaction assays, respectively. The CCK‑8 assay demonstrated that HTY contributed to HUVEC proliferation mediated by PEMFs in a time‑dependent manner. The Transwell assay and scratch wound results demonstrated that co‑treatment of HTY and PEMFs could increase HUVEC migration. Furthermore, the levels of apoptotic cells were reversed by pre‑incubation with HTY in the PEMF treatment group, while PEMF treatment alone had no such effect. The proteins and mRNA expression levels of Akt, mTOR, TGF‑β1 were elevated in co‑treatment of HTY and PEMFs, whereas there was no effect on levels of p53. Therefore, the results indicated that combined exposure of HUVECs to PEMFs and HTY exerted protective effects in HUVECs by promoting cell proliferation and inhibiting apoptosis. In conclusion, to the best of our knowledge, the present study was the first to demonstrate the beneficial roles of HTY and PEMF combined treatment in HUVECs, which may represent an effective treatment for wound healing.

2260 related Products with: Hydroxytyrosol contributes to cell proliferation and inhibits apoptosis in pulsed electromagnetic fields treated human umbilical vein endothelial cells in vitro.

Human Umbilical Vein Endo GFP Expressing Human Umbi Mitochondria GFP Tag Huma Plasma Membrane GFP Tag H RFP Expressing Human Umbi Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Macrophage Colony Stimula Macrophage Colony Stimula Cultrex In Vitro Angiogen

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#28983072   2017/10/06 Save this To Up

Raf Kinase Inhibitor Protein (RKIP) Inhibits Tumor Necrosis Factor-α (TNF-α) Induced Adhesion Molecules Expression in Vascular Smooth Muscle Bells by Suppressing (Nuclear Transcription Factor-κB (NF-kappaB) Pathway.

BACKGROUND Raf kinase inhibitor protein (RKIP) regulates growth and differentiation and plays a role in key signal transduction cascades in mammalian cells. Nevertheless, the underlying mechanism for which RKIP regulates cell-cell adhesion remains unknown. Our study investigated the function of the RKIP overexpression on adhesion molecules expression induced by tumor necrosis factor (TNF)-α in cultured mouse vascular smooth muscle cells (MOVACs). MATERIAL AND METHODS The expression levels of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were detected by ELISA kit, reverse transcription-PCR, and western blot assays. The protein expression of RKIP, p65, and inhibitor of nuclear factor (NF)-κBα (IκBα) were detected by western blot analysis. The activity of NF-kappaB was determined using a Dual-Luciferase Reporter assay. RESULTS The results showed that MOVACs transfected with pCMV5-HA-RKIP significantly inhibited TNF-α induced mRNA and protein expression of ICAM-1 and VCAM-1. The adhesion of THP-1 cells was also detected and inhibited by pCMV5-HA-RKIP in TNF-α-treated MOVACs. RKIP also suppressed the TNF-α-induced activation of NF-kappaB and the protein expression of phosphorylated IκB-α, and promoted the protein expression of IkB-α and nuclear translocation of p65 NF-kappaB. Furthermore, RKIP and the inhibitor of NF-kappaB (BAY11-7082) reduced the upregulation of ICAM-1 and VACM-1 induced by TNF-α. CONCLUSIONS Taken together, these results suggested that RKIP may inhibit the TNF-α-induced expression of adhesion molecules in MOVACs through inactivation of the NF-kappaB pathway.

2395 related Products with: Raf Kinase Inhibitor Protein (RKIP) Inhibits Tumor Necrosis Factor-α (TNF-α) Induced Adhesion Molecules Expression in Vascular Smooth Muscle Bells by Suppressing (Nuclear Transcription Factor-κB (NF-kappaB) Pathway.

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#28962172   2017/09/30 Save this To Up

Psoralen stimulates osteoblast proliferation through the activation of nuclear factor-κB-mitogen-activated protein kinase signaling.

Osteoporosis is a systemic skeletal disease that leads to increased bone fragility and susceptibility to fracture. Approximately 50% of postmenopausal women develop osteoporosis as a result of postmenopausal estrogen deficiency. To reduce fractures related to osteoporosis in women, previous studies have focused on therapeutic strategies that aim to increase bone formation or decrease bone resorption. However, pharmacological agents that aim to improve bone fracture susceptibility exhibit side effects. Current studies are investigating natural alternatives that possess the benefits of selective estrogen receptor modulators (SERMs) without the adverse effects. Recent studies have indicated that phytoestrogen may be an ideal natural SERM for the treatment of osteoporosis. In Chinese herbal medicine, psoralen, as the predominant substance of Psoralea corylifolia, is considered to be a phytoestrogen and is used as a remedy for osteoporosis. A number of studies have demonstrated the efficacy of psoralen in bone formation. However, the pathways and underlying molecular mechanisms that participate in psoralen-induced osteoblast formation are not well understood. In the present study, hFOB1.19 cells were treated with psoralen at different concentrations (0, 5, 10, 15 and 20 µM) for 0, 24, 36, 48 and 72 h, respectively. Reverse transcription-quantitative polymerase chain reaction and western blot assays were performed to detect glucose transporter 3 (GLUT3) expression. A cell counting kit-8 assay was used to analyze cell proliferation. In addition the effects of mitogen activated protein kinase inhibitors on extracellular signal-regulated kinase (ERK), phosphorylated (p)-ERK, p38, p-p38, c-Jun N-terminal kinase (JNK) and p-JNK expressions and cell proliferation were measured, as was the effect of nuclear factor (NF)-κB inhibitor on P65 and GLUT3 expressions and cell proliferation. The results indicated that psoralen stimulates hFOB1.19 cell proliferation in a dose-dependent manner (P<0.05). Phospho-ERK, p38 and JNK were markedly increased by psoralen compared with the control group (P<0.05), and the specific inhibitors of ERK (SCH772984), p38 (SB203580) and JNK (SP600125) reversed the stimulatory effects of psoralen on signal marker phosphorylation (P<0.05). The rate of psoralen-induced cell proliferation was significantly suppressed by inhibitors of ERK, JNK and p38 compared with psoralen treatment alone (P<0.05). In addition, psoralen stimulated osteoblast proliferation via the NF-κB signaling pathway. Therefore, the present findings suggest that psoralen may be a potential natural alternative to SERMs in the treatment of osteoporosis and fractures.

1845 related Products with: Psoralen stimulates osteoblast proliferation through the activation of nuclear factor-κB-mitogen-activated protein kinase signaling.

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#28960265   2017/09/29 Save this To Up

Cabozantinib is well tolerated in acute myeloid leukemia and effectively inhibits the resistance-conferring FLT3/tyrosine kinase domain/F691 mutation.

Cabozantinib, a tyrosine kinase inhibitor of FMS-like tyrosine kinase 3 (FLT3), MET, AXL, vascular endothelial growth factor receptor, and KIT, is approved for use in multiple malignancies. We assessed the safety and tolerability of cabozantinib in AML, given up-regulation of multiple relevant pathways.

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