1,749,466 research outputs found
Table2_miR-654-5p Contributes to the Activation and Proliferation of Hepatic Stellate Cells by Targeting RXRα.XLSX
No full textLiver fibrosis (LF) is a major disease that threatens human health. Hepatic stellate cells (HSCs) contribute directly to LF via extracellular matrix (ECM) secretion. Moreover, RXRα is an important nuclear receptor that plays a key regulatory role in HSC activation. Meanwhile, microRNAs (miRNAs) have been identified as significant regulators of LF development. In particular, miR-654-5p is involved in cellular migration and proliferation, and via bioinformatics analysis, has been identified as a potential factor that targets RXRα in humans and in mice. However, the precise relationship between miR-654-5p and RXRα in the context of LF, remains unknown and is the primary focus of the current study. To establish in vitro activated cell model human primary HSCs were cultured in vitro and LX-2 cells were stimulated with recombinant human TGF-β1. mRNA and protein levels of RXRα, miR-654-5p and fibrogenic genes were compared in quiescent and activated HSCs. Moreover, after transfected with miR-654-5p mimics, the expression changes of above related genes in LX-2 cells were estimated. Meanwhile, cell proliferation and apoptosis were detected in miR-654-5p overexpressed LX-2 cells. Simultaneously, the targeted binding between miR-654-5p and RXRα was verified in LX-2 cells. Carbon tetrachloride (CCl4)-induced mouse model with liver fibrosis was use to research the role of the miR-654-5p in vitro. Our results show that miR-654-5p expression levels increased in activated human HSCs and TGFβ-treated LX-2 cells. Moreover, miR-654-5p mimics markedly promoted LX-2 cell proliferation while inhibiting their apoptosis. Accordingly, the expression levels of RXRα are decreased in activated HSCs and LX-2 cells. Additionally, dual-luciferase reporter assay results reveal direct targeting of RXRα by miR-654-5p. Similarly, in vivo miR-654-5p overexpression aggravates LF in mice that are intraperitoneally injected with CCl4. Taken together, our findings elucidated a novel molecular mechanism with potential use for treatment of LF.</p
Image3_miR-654-5p Contributes to the Activation and Proliferation of Hepatic Stellate Cells by Targeting RXRα.JPEG
No full textLiver fibrosis (LF) is a major disease that threatens human health. Hepatic stellate cells (HSCs) contribute directly to LF via extracellular matrix (ECM) secretion. Moreover, RXRα is an important nuclear receptor that plays a key regulatory role in HSC activation. Meanwhile, microRNAs (miRNAs) have been identified as significant regulators of LF development. In particular, miR-654-5p is involved in cellular migration and proliferation, and via bioinformatics analysis, has been identified as a potential factor that targets RXRα in humans and in mice. However, the precise relationship between miR-654-5p and RXRα in the context of LF, remains unknown and is the primary focus of the current study. To establish in vitro activated cell model human primary HSCs were cultured in vitro and LX-2 cells were stimulated with recombinant human TGF-β1. mRNA and protein levels of RXRα, miR-654-5p and fibrogenic genes were compared in quiescent and activated HSCs. Moreover, after transfected with miR-654-5p mimics, the expression changes of above related genes in LX-2 cells were estimated. Meanwhile, cell proliferation and apoptosis were detected in miR-654-5p overexpressed LX-2 cells. Simultaneously, the targeted binding between miR-654-5p and RXRα was verified in LX-2 cells. Carbon tetrachloride (CCl4)-induced mouse model with liver fibrosis was use to research the role of the miR-654-5p in vitro. Our results show that miR-654-5p expression levels increased in activated human HSCs and TGFβ-treated LX-2 cells. Moreover, miR-654-5p mimics markedly promoted LX-2 cell proliferation while inhibiting their apoptosis. Accordingly, the expression levels of RXRα are decreased in activated HSCs and LX-2 cells. Additionally, dual-luciferase reporter assay results reveal direct targeting of RXRα by miR-654-5p. Similarly, in vivo miR-654-5p overexpression aggravates LF in mice that are intraperitoneally injected with CCl4. Taken together, our findings elucidated a novel molecular mechanism with potential use for treatment of LF.</p
Image2_miR-654-5p Contributes to the Activation and Proliferation of Hepatic Stellate Cells by Targeting RXRα.JPEG
No full textLiver fibrosis (LF) is a major disease that threatens human health. Hepatic stellate cells (HSCs) contribute directly to LF via extracellular matrix (ECM) secretion. Moreover, RXRα is an important nuclear receptor that plays a key regulatory role in HSC activation. Meanwhile, microRNAs (miRNAs) have been identified as significant regulators of LF development. In particular, miR-654-5p is involved in cellular migration and proliferation, and via bioinformatics analysis, has been identified as a potential factor that targets RXRα in humans and in mice. However, the precise relationship between miR-654-5p and RXRα in the context of LF, remains unknown and is the primary focus of the current study. To establish in vitro activated cell model human primary HSCs were cultured in vitro and LX-2 cells were stimulated with recombinant human TGF-β1. mRNA and protein levels of RXRα, miR-654-5p and fibrogenic genes were compared in quiescent and activated HSCs. Moreover, after transfected with miR-654-5p mimics, the expression changes of above related genes in LX-2 cells were estimated. Meanwhile, cell proliferation and apoptosis were detected in miR-654-5p overexpressed LX-2 cells. Simultaneously, the targeted binding between miR-654-5p and RXRα was verified in LX-2 cells. Carbon tetrachloride (CCl4)-induced mouse model with liver fibrosis was use to research the role of the miR-654-5p in vitro. Our results show that miR-654-5p expression levels increased in activated human HSCs and TGFβ-treated LX-2 cells. Moreover, miR-654-5p mimics markedly promoted LX-2 cell proliferation while inhibiting their apoptosis. Accordingly, the expression levels of RXRα are decreased in activated HSCs and LX-2 cells. Additionally, dual-luciferase reporter assay results reveal direct targeting of RXRα by miR-654-5p. Similarly, in vivo miR-654-5p overexpression aggravates LF in mice that are intraperitoneally injected with CCl4. Taken together, our findings elucidated a novel molecular mechanism with potential use for treatment of LF.</p
Image1_miR-654-5p Contributes to the Activation and Proliferation of Hepatic Stellate Cells by Targeting RXRα.JPEG
No full textLiver fibrosis (LF) is a major disease that threatens human health. Hepatic stellate cells (HSCs) contribute directly to LF via extracellular matrix (ECM) secretion. Moreover, RXRα is an important nuclear receptor that plays a key regulatory role in HSC activation. Meanwhile, microRNAs (miRNAs) have been identified as significant regulators of LF development. In particular, miR-654-5p is involved in cellular migration and proliferation, and via bioinformatics analysis, has been identified as a potential factor that targets RXRα in humans and in mice. However, the precise relationship between miR-654-5p and RXRα in the context of LF, remains unknown and is the primary focus of the current study. To establish in vitro activated cell model human primary HSCs were cultured in vitro and LX-2 cells were stimulated with recombinant human TGF-β1. mRNA and protein levels of RXRα, miR-654-5p and fibrogenic genes were compared in quiescent and activated HSCs. Moreover, after transfected with miR-654-5p mimics, the expression changes of above related genes in LX-2 cells were estimated. Meanwhile, cell proliferation and apoptosis were detected in miR-654-5p overexpressed LX-2 cells. Simultaneously, the targeted binding between miR-654-5p and RXRα was verified in LX-2 cells. Carbon tetrachloride (CCl4)-induced mouse model with liver fibrosis was use to research the role of the miR-654-5p in vitro. Our results show that miR-654-5p expression levels increased in activated human HSCs and TGFβ-treated LX-2 cells. Moreover, miR-654-5p mimics markedly promoted LX-2 cell proliferation while inhibiting their apoptosis. Accordingly, the expression levels of RXRα are decreased in activated HSCs and LX-2 cells. Additionally, dual-luciferase reporter assay results reveal direct targeting of RXRα by miR-654-5p. Similarly, in vivo miR-654-5p overexpression aggravates LF in mice that are intraperitoneally injected with CCl4. Taken together, our findings elucidated a novel molecular mechanism with potential use for treatment of LF.</p
Image8_MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis.TIF
No full textBackground: MiR-654-3p can repress malignant progression of cancer cells, whereas no relative reports were about its modulatory mechanism in sinonasal squamous cell carcinoma (SNSCC). This research committed to approaching modulatory effect of miR-654-3p on SNSCC cells.Methods: Bioinformatics methods were utilized for analyzing interaction of miR-654-3p/cAMP-responsive element binding protein 1 (CREB1)/presenilin-1 (PSEN1). Expression levels of miR-654-3p, CREB1, and PSEN1 mRNA were assessed by quantitative real-time polymerase chain reaction. Western blot was completed for level assessment of CREB1, PSEN1, and epithelial–mesenchymal transition–related proteins. The targeted relationship between miR-654-3p and CREB1, or CREB1 and PSEN1 was authenticated via dual-luciferase assay and ChIP assay. A trail of experiments in vitro was used for detection of the effects of miR-654-3p/CREB1/PSEN1 axis on malignant progression of SNSCC cells.Results: CREB1 as the downstream target mRNA of miR-654-3p could activate transcription of its downstream target gene PSEN1. Besides, miR-654-3p could target CREB1 to repress PSEN1 expression, thus restraining proliferation, migration, invasion, epithelial–mesenchymal transition, and hastening apoptosis of SNSCC cells.Conclusion: MiR-654-3p as an antitumor gene targeted CREB1 to hamper malignant progression of SNSCC through miR-654-3p/CREB1/PSEN1 axis.</p
Table1_MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis.XLSX
No full textBackground: MiR-654-3p can repress malignant progression of cancer cells, whereas no relative reports were about its modulatory mechanism in sinonasal squamous cell carcinoma (SNSCC). This research committed to approaching modulatory effect of miR-654-3p on SNSCC cells.Methods: Bioinformatics methods were utilized for analyzing interaction of miR-654-3p/cAMP-responsive element binding protein 1 (CREB1)/presenilin-1 (PSEN1). Expression levels of miR-654-3p, CREB1, and PSEN1 mRNA were assessed by quantitative real-time polymerase chain reaction. Western blot was completed for level assessment of CREB1, PSEN1, and epithelial–mesenchymal transition–related proteins. The targeted relationship between miR-654-3p and CREB1, or CREB1 and PSEN1 was authenticated via dual-luciferase assay and ChIP assay. A trail of experiments in vitro was used for detection of the effects of miR-654-3p/CREB1/PSEN1 axis on malignant progression of SNSCC cells.Results: CREB1 as the downstream target mRNA of miR-654-3p could activate transcription of its downstream target gene PSEN1. Besides, miR-654-3p could target CREB1 to repress PSEN1 expression, thus restraining proliferation, migration, invasion, epithelial–mesenchymal transition, and hastening apoptosis of SNSCC cells.Conclusion: MiR-654-3p as an antitumor gene targeted CREB1 to hamper malignant progression of SNSCC through miR-654-3p/CREB1/PSEN1 axis.</p
Image4_MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis.TIF
No full textBackground: MiR-654-3p can repress malignant progression of cancer cells, whereas no relative reports were about its modulatory mechanism in sinonasal squamous cell carcinoma (SNSCC). This research committed to approaching modulatory effect of miR-654-3p on SNSCC cells.Methods: Bioinformatics methods were utilized for analyzing interaction of miR-654-3p/cAMP-responsive element binding protein 1 (CREB1)/presenilin-1 (PSEN1). Expression levels of miR-654-3p, CREB1, and PSEN1 mRNA were assessed by quantitative real-time polymerase chain reaction. Western blot was completed for level assessment of CREB1, PSEN1, and epithelial–mesenchymal transition–related proteins. The targeted relationship between miR-654-3p and CREB1, or CREB1 and PSEN1 was authenticated via dual-luciferase assay and ChIP assay. A trail of experiments in vitro was used for detection of the effects of miR-654-3p/CREB1/PSEN1 axis on malignant progression of SNSCC cells.Results: CREB1 as the downstream target mRNA of miR-654-3p could activate transcription of its downstream target gene PSEN1. Besides, miR-654-3p could target CREB1 to repress PSEN1 expression, thus restraining proliferation, migration, invasion, epithelial–mesenchymal transition, and hastening apoptosis of SNSCC cells.Conclusion: MiR-654-3p as an antitumor gene targeted CREB1 to hamper malignant progression of SNSCC through miR-654-3p/CREB1/PSEN1 axis.</p
Image5_MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis.TIF
No full textBackground: MiR-654-3p can repress malignant progression of cancer cells, whereas no relative reports were about its modulatory mechanism in sinonasal squamous cell carcinoma (SNSCC). This research committed to approaching modulatory effect of miR-654-3p on SNSCC cells.Methods: Bioinformatics methods were utilized for analyzing interaction of miR-654-3p/cAMP-responsive element binding protein 1 (CREB1)/presenilin-1 (PSEN1). Expression levels of miR-654-3p, CREB1, and PSEN1 mRNA were assessed by quantitative real-time polymerase chain reaction. Western blot was completed for level assessment of CREB1, PSEN1, and epithelial–mesenchymal transition–related proteins. The targeted relationship between miR-654-3p and CREB1, or CREB1 and PSEN1 was authenticated via dual-luciferase assay and ChIP assay. A trail of experiments in vitro was used for detection of the effects of miR-654-3p/CREB1/PSEN1 axis on malignant progression of SNSCC cells.Results: CREB1 as the downstream target mRNA of miR-654-3p could activate transcription of its downstream target gene PSEN1. Besides, miR-654-3p could target CREB1 to repress PSEN1 expression, thus restraining proliferation, migration, invasion, epithelial–mesenchymal transition, and hastening apoptosis of SNSCC cells.Conclusion: MiR-654-3p as an antitumor gene targeted CREB1 to hamper malignant progression of SNSCC through miR-654-3p/CREB1/PSEN1 axis.</p
Image9_MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis.TIF
No full textBackground: MiR-654-3p can repress malignant progression of cancer cells, whereas no relative reports were about its modulatory mechanism in sinonasal squamous cell carcinoma (SNSCC). This research committed to approaching modulatory effect of miR-654-3p on SNSCC cells.Methods: Bioinformatics methods were utilized for analyzing interaction of miR-654-3p/cAMP-responsive element binding protein 1 (CREB1)/presenilin-1 (PSEN1). Expression levels of miR-654-3p, CREB1, and PSEN1 mRNA were assessed by quantitative real-time polymerase chain reaction. Western blot was completed for level assessment of CREB1, PSEN1, and epithelial–mesenchymal transition–related proteins. The targeted relationship between miR-654-3p and CREB1, or CREB1 and PSEN1 was authenticated via dual-luciferase assay and ChIP assay. A trail of experiments in vitro was used for detection of the effects of miR-654-3p/CREB1/PSEN1 axis on malignant progression of SNSCC cells.Results: CREB1 as the downstream target mRNA of miR-654-3p could activate transcription of its downstream target gene PSEN1. Besides, miR-654-3p could target CREB1 to repress PSEN1 expression, thus restraining proliferation, migration, invasion, epithelial–mesenchymal transition, and hastening apoptosis of SNSCC cells.Conclusion: MiR-654-3p as an antitumor gene targeted CREB1 to hamper malignant progression of SNSCC through miR-654-3p/CREB1/PSEN1 axis.</p
Image6_MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis.TIF
No full textBackground: MiR-654-3p can repress malignant progression of cancer cells, whereas no relative reports were about its modulatory mechanism in sinonasal squamous cell carcinoma (SNSCC). This research committed to approaching modulatory effect of miR-654-3p on SNSCC cells.Methods: Bioinformatics methods were utilized for analyzing interaction of miR-654-3p/cAMP-responsive element binding protein 1 (CREB1)/presenilin-1 (PSEN1). Expression levels of miR-654-3p, CREB1, and PSEN1 mRNA were assessed by quantitative real-time polymerase chain reaction. Western blot was completed for level assessment of CREB1, PSEN1, and epithelial–mesenchymal transition–related proteins. The targeted relationship between miR-654-3p and CREB1, or CREB1 and PSEN1 was authenticated via dual-luciferase assay and ChIP assay. A trail of experiments in vitro was used for detection of the effects of miR-654-3p/CREB1/PSEN1 axis on malignant progression of SNSCC cells.Results: CREB1 as the downstream target mRNA of miR-654-3p could activate transcription of its downstream target gene PSEN1. Besides, miR-654-3p could target CREB1 to repress PSEN1 expression, thus restraining proliferation, migration, invasion, epithelial–mesenchymal transition, and hastening apoptosis of SNSCC cells.Conclusion: MiR-654-3p as an antitumor gene targeted CREB1 to hamper malignant progression of SNSCC through miR-654-3p/CREB1/PSEN1 axis.</p
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