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Total 1545 results found since Jan 2013.

Overexpression of Long Non-Coding RNA TUG1 Promotes Colon Cancer Progression.
CONCLUSIONS LncRNA TUG1 may serve as a potential oncogene for colon cancer. Overexpressed TUG1 may contribute to promoting cell proliferation and migration in colon cancer cells. PMID: 27634385 [PubMed - in process]
Source: Medical Science Monitor - September 19, 2016 Category: Research Tags: Med Sci Monit Source Type: research

Long Non-Coding RNA (lncRNA) Urothelial Carcinoma-Associated 1 (UCA1) Enhances Tamoxifen Resistance in Breast Cancer Cells via Inhibiting mTOR Signaling Pathway.
CONCLUSIONS UCA1 upregulation was associated with tamoxifen resistance in breast cancer. Mechanistically, UCA1 confers tamoxifen resistance to breast cancer cells partly via activating the mTOR signaling pathway. PMID: 27765938 [PubMed - in process]
Source: Medical Science Monitor - October 23, 2016 Category: Research Tags: Med Sci Monit Source Type: research

Aberrant Expression of microRNA-9 Contributes to Development of Intracranial Aneurysm by Suppressing Proliferation and Reducing Contractility of Smooth Muscle Cells.
CONCLUSIONS Our findings show that dysregulation of miR-9 is responsible for the development of IA via targeting MYOCD. miR-9 and its direct target, MYOCD, might novel therapeutic targets in the treatment of IA. PMID: 27824808 [PubMed - in process]
Source: Medical Science Monitor - November 10, 2016 Category: Research Tags: Med Sci Monit Source Type: research

AGE/RAGE promotes thecalcification of human aortic smooth muscle cells via the Wnt/ β-catenin axis.
CONCLUSION: Increased expression of RAGE promoted calcification in HASMCs and up regulated the β-catenin, OPG and Cbfa1 genes. RAGE may activate the downstream genes via the Wntβ-catenin pathway, thereby promoting HASMC differentiation into osteogenic cells and calcification. PMID: 27904668 [PubMed - in process]
Source: American Journal of Translational Research - December 3, 2016 Category: Research Tags: Am J Transl Res Source Type: research

TGF- β1/Smad3 Signaling Pathway Suppresses Cell Apoptosis in Cerebral Ischemic Stroke Rats.
CONCLUSIONS The TGF-β1/Smad3 signaling pathway was up-regulated once cerebral ischemic stroke was simulated. TGF-β1 may activate the expression of Bcl-2 via Smad3 to suppress the apoptosis of neurons. PMID: 28110342 [PubMed - in process]
Source: Medical Science Monitor - January 25, 2017 Category: Research Tags: Med Sci Monit Source Type: research

FBP1 is Highly Expressed in Human Hypertrophic Scars and Increases Fibroblast Proliferation, Apoptosis and Collagen Expression.
CONCLUSION: FBP1 is highly expressed in human hypertrophic scars and increases fibroblast proliferation, apoptosis and collagen expression. PMID: 28362515 [PubMed - as supplied by publisher]
Source: Connective Tissue Research - April 2, 2017 Category: Research Tags: Connect Tissue Res Source Type: research

Reduced monocyte adhesion to aortae of diabetic plasminogen activator inhibitor-1 knockout mice
ConclusionThe findings suggest that PAI-1 is required for diabetes-induced monocyte adhesion via interactions with uPA/uPAR, and it also regulates TLR4 and TNF α expression in vascular EC. Inhibition of PAI-1 potentially reduces vascular inflammation under diabetic condition.
Source: Inflammation Research - May 26, 2017 Category: Research Source Type: research

MiR-31 is involved in the high glucose-suppressed osteogenic differentiation of human periodontal ligament stem cells by targeting Satb2.
In this study, we found that diabetic mice with increased miR-31 level in periodontal ligaments exhibited greater bone loss. In vitro, the high expression of miR-31 is associated with the impaired osteogenic differentiation ability of PDLSCs in high glucose environment. Furthermore, miR-31 inhibitors increased mineralized bone matrix formation and raised Runx2, Osx and OCN expression at both mRNA and protein levels. However, PDLSCs pretreated with miR-31 mimics decreased bone matrix formation and reduced Runx2, Osx and OCN expression level in high glucose microenvironment. Moreover, Satb2 was identified as a target of miR-...
Source: American Journal of Translational Research - June 2, 2017 Category: Research Tags: Am J Transl Res Source Type: research

Interaction of Wip1 and NF- κB regulates neuroinflammatory response in astrocytes
ConclusionThese data provide a mechanism for the role for a negative feedback loop of Wip1 and NF- κB in LPS-induced astrocytic activation.
Source: Inflammation Research - August 5, 2017 Category: Research Source Type: research

Synergistic Effect of Notch-3-Specific Inhibition and Paclitaxel in Non-Small Cell Lung Cancer (NSCLC) Cells Via Activation of The Intrinsic Apoptosis Pathway.
CONCLUSIONS These results indicate a synergistic effect of Notch-3-specific inhibition and paclitaxel through alteration of the intrinsic apoptosis pathway, which was involved in Notch-3-induced chemoresistance in NSCLC cells, and GSI inhibited Notch-3-induced chemoresistance in a concentration-dependent manner. This approach that combines Notch-3-specific inhibition and paclitaxel would be likely to apply in NSCLC. PMID: 28769027 [PubMed - in process]
Source: Medical Science Monitor - August 6, 2017 Category: Research Tags: Med Sci Monit Source Type: research

Decreasing Eukaryotic Initiation Factor 3C (EIF3C) Suppresses Proliferation and Stimulates Apoptosis in Breast Cancer Cell Lines Through Mammalian Target of Rapamycin (mTOR) Pathway.
CONCLUSIONS Unveiling the mechanisms of EIF3 action in tumorigenesis may help identify attractive targets for cancer therapy. PMID: 28854163 [PubMed - in process]
Source: Medical Science Monitor - September 1, 2017 Category: Research Tags: Med Sci Monit Source Type: research

Toll-Like Receptor 4 Reduces Occludin and Zonula Occludens 1 to Increase Retinal Permeability Both in vitro < b > < /b > and in vivo
In conclusion, these studies demonstrate that TLR4 in EC strongly regulates retinal permeability and neuronal and vasc ular changes following exposure to stressors such as I/R.J Vasc Res 2017;54:367-375
Source: Journal of Vascular Research - November 14, 2017 Category: Research Source Type: research

Activation of Therapeutic Functionalities with Chimeric RNA/DNA Nanoparticles for Treatment of Cancer, Viruses and Other Diseases
A new strategy based on RNA/DNA hybrid nanoparticles, which can be generally used for triggering multiple functionalities inside diseased cells is presented. Individually, each of the hybrids is functionally inactive and functional representation can only be activated by the re-association of at least two cognate hybrids simultaneously present in the same cell. Overall, this novel approach allows (i) the triggered release of therapeutic siRNAs or miRNAs inside the diseased cells, (ii) activation of other split functionalities (e.g. FRET, different aptamers, rybozymes, split proteins) intracellularly, (iii) higher control o...
Source: NIH OTT Licensing Opportunities - December 8, 2017 Category: Research Authors: ajoyprabhu3 Source Type: research

Inhibition of N-acetyltransferase 10 using remodelin attenuates doxorubicin resistance by reversing the epithelial-mesenchymal transition in breast cancer.
Authors: Wu J, Zhu H, Wu J, Chen W, Guan X Abstract Development of resistance to doxorubicin-based chemotherapy limits curative effect in breast cancer (BC). N-acetyltransferase 10 (NAT10), a nucleolar protein involved in histone acetylation, is overexpressed in several cancers. We investigated whether NAT10 is involved in doxorubicin resistance in BC and explored the potential mechanisms. Remodelin, a NAT10 inhibitor, and a NAT10 small interfering RNA (siRNA) were used to inhibit NAT10; both remodelin and the NAT10 siRNA reduced cell viability and attenuated doxorubicin resistance in four BC cell lines. Remodelin ...
Source: American Journal of Translational Research - February 11, 2018 Category: Research Tags: Am J Transl Res Source Type: research

Steroid Receptor Coactivator-Interacting Protein (SIP) Suppresses Myocardial Injury Caused by Acute Pancreatitis.
CONCLUSIONS In conclusion, the results suggested that SIP may inhibit the inflammatory response by deactivating p65, thus reducing the myocardial damage caused by AP. PMID: 29765014 [PubMed - in process]
Source: Medical Science Monitor - May 18, 2018 Category: Research Tags: Med Sci Monit Source Type: research