- Chinese︱Feedback︱Save this page
Get RSS feed
Check out RSS, or use RSS reader to subscribe this item 
Confirmation
Authentication email has already been sent, please check your email box: and activate it as soon as possible.
You can login to My Profile and manage your email alerts.
If you haven’t received the email, please:
- Login︱Register
|
|
|
 |
|
||
| There are 13 papers published in subject: > since this site started. | |||
| Select Subject |
| Select/Unselect all | For Selected Papers |
Saved Papers
Please enter a name for this paper to be shown in your personalized Saved Papers list
|
 |
| 1. Ginsenoside-Rh2 suppresses proliferation and migration of hepatocellular carcinoma cells by targeting EZH2 to regulate CDKN2A-2B gene cluster transcription | |||
| Li Qi | |||
| Basic Medicine 25 April 2017 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Ginsenoside-Rh2 (G-Rh2) exerts important pharmacological effects with regard to the control of human hepatocellular carcinoma (HCC). EZH2 is a potent histone methyltransferase of H3K27me3, which has been determined as an oncogene in many malignancies. The CDKN2A-2B gene cluster encodes three important tumor suppressors, P14, P15 and P16. In this study, the anticancer effect and molecular mechanism of G-Rh2 on HCC was investigated. Treatment of HCC cells with G-Rh2 inhibited cell proliferation, migration and induced cell cycle arrest at the G0/G1 phase. We demonstrate for the first time that this effect was specifically mediated by down-regulating expression of EZH2. Further molecular mechanism study indicated that the decreased EZH2 promoted P14, P15 and P16 gene transcription through reducing H3K27me3 modification in the promoter of CDKN2A-2B gene cluster loci. Similarly, silencing of EZH2 by siRNA down-regulated P14, P15, P16 mRNA levels and inhibited HCC cell proliferation. Our results suggested that EZH2 could be a potentially therapeutic target by G-Rh2 in HCC, which provided a rationale for the development of drugs that inhibited histone methylase as a strategy against various cancers. | |||
| TO cite this article:Li Qi. Ginsenoside-Rh2 suppresses proliferation and migration of hepatocellular carcinoma cells by targeting EZH2 to regulate CDKN2A-2B gene cluster transcription[OL].[25 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4727383 | |||
| 2. Early detection in urinary proteome for the effective early treatment of bleomycin-induced pulmonary fibrosis in a rat model | |||
| WU Jianqiang,LI Xundou,GAO Youhe | |||
| Basic Medicine 10 January 2017 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal fibrotic lung disease. With limited effective treatments available in the late stage, IPF has a very poor prognosis, with an average survival time of under 3 years. Molecular biomarkers are highly desired for IPF, especially for its early phase. Lacking homeostatic control, urine is a better biomarker source than blood for detecting small and early pathological changes.In this study, urine samples were collected from rats with bleomycin-induced pulmonary fibrosis. Samples collected during slight fibrosis were used for early diagnostic biomarker identification; 11 differentially expressed proteins were identified by labeled proteome quantitation, four of which were previously reported to be associated with fibrosis. In samples during fibrosis progression, 30 differentially expressed proteins were identified as biomarkers for disease monitoring, many of which have been reported to be associated with IPF pathogenesis. Then, prednisone treatment was administered at different phases of fibrosis. Early prednisone treatment effectively inhibited pulmonary fibrosis, whereas the same treatment later had very limited effects. Trends in the change of 5 differentially expressed proteins were reversed after prednisone treatment, indicating that these proteins could serve as biomarkers of therapeutic response.Urinary proteomics has been underutilized in respiratory diseases. This is the first application of urinary proteomics to pulmonary fibrosis. Urine proteins could enable early diagnosis and monitoring of both disease progression and treatment efficacy in IPF and probably in other pulmonary diseases. These findings may improve our understanding of the pathogenesis of pulmonary fibrosis. | |||
| TO cite this article:WU Jianqiang,LI Xundou,GAO Youhe. Early detection in urinary proteome for the effective early treatment of bleomycin-induced pulmonary fibrosis in a rat model[OL].[10 January 2017] http://en.paper.edu.cn/en_releasepaper/content/4716803 | |||
| 3. Oncogenetic natural antisense transcript, PTB-AS, promotes glioma cancer by elevating the expression of PTB | |||
| Zhu liyuan,Ruan Xiangbin,Wu Fan,Qi Yingjiao,Zhou junjie,Liu Wei,Li liang,Zhang jing,Yin Bin,Jiang Tao,Yuan Jiangang,Qiang Boqin,Han Wei,Peng Xiaozhong | |||
| Basic Medicine 12 March 2016 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Glioma is the most common primary malignancy in the brain, which has the high recurrence and lethality rate, and it's imminent to explore the molecular mechanism of this incurable disease. Poly-pyrimidine tract binding protein (PTB, also known as PTBP1) is a kind of RNA-binding protein with various molecular functions and plays an indispensable role in glioma. Since research about the regulation of PTB is limited in microRNAs and transcription factors, here we want to explore the new lncRNA regulators of PTB in order to consummate the principle of controlling the PTB expression and further reveal the molecular mechanism of accommodating glioma tumorigenesis. We identify a novel natural antisense transcript of PTB named PTB-AS and find that the expression of PTB-AS in glioma is significantly directly correlated with PTB-mRNA. Naturally, knocking down the abundance of PTB-AS in glioma can remarkably reduce the expression of PTB mRNA and protein. Then we validate the important function of PTB-AS in glioma for the first time and discover the original fact that PTB-AS influence the stability of PTB-mRNA by directly binding to PTB-3'UTR, what's more, it's the latest finding to demonstrate that miR-9 can negatively regulate PTB in human cancer and in practice PTB-AS could elevate the expression of PTB by masking the binding site of miR-9 in PTB-3'UTR so as to maintain the high expression level of PTB, miR-9 and itself in glioma. | |||
| TO cite this article:Zhu liyuan,Ruan Xiangbin,Wu Fan, et al. Oncogenetic natural antisense transcript, PTB-AS, promotes glioma cancer by elevating the expression of PTB[OL].[12 March 2016] http://en.paper.edu.cn/en_releasepaper/content/4680311 | |||
| 4. 17β-Estradiol Up-Regulates NRF2 via PI3k/AKT and Estrogen Receptor Signaling Pathways to Suppress Light-Induced Retinal Degeneration in Rat | |||
| ZHU Chunhui,LI Hongbo,WANG Shaolan,WANG Baoying,HU Chenghu,DU Fangying,ZHAO Panpan,LI Ang,YU Xiaorui | |||
| Basic Medicine 17 June 2015 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Human age-related retinal diseases, such as age-related macular degeneration (AMD), are intimately associated with decreased tissue oxygenation and hypoxia. Different antioxidants have been investigated to reverse AMD. In the present study, we describe the antioxidant 17β-estradiol (βE2) and investigate its protective effects on retinal neurons. Fourteen days after ovariectomy, adult Sprague-Dawley rats were exposed to 8000-lux light for 12 h to induce retinal degeneration. Reactive oxygen species (ROS) levels were assessed by confocal fluorescence microscopy using 2, 7-dichlorofluorescein diacetate. Nuclear factor erythroid 2-related factor 2 (Nrf2) and antioxidant enzyme mRNA expression were detected by real-time PCR. Western blotting was used to evaluate NRF2 activation. NRF2 translocation was determined by immunohistochemistry, with morphological changes monitored by hematoxylin and eosin staining. Following light exposure, βE2 significantly reduced ROS production. βE2 also up-regulated NRF2 mRNA and protein levels, with maximal expression at 4 and 12h post-exposure, respectively. Interestingly, following βE2 administration, NRF2 was translocated from the cytoplasm to the nucleus, primarily in the outer nuclear layer. βE2 also up-regulated NRF2, which triggered phase-2 antioxidant enzyme expression (superoxide dismutases 1 and 2, catalase, glutaredoxins 1 and 2, and thioredoxins 1 and 2), reduced ROS production, and ameliorated retinal damage. However, the beneficial effects of βE2 were markedly suppressed by pretreatment with LY294002 or ICI182780, specific inhibitors of the phosphotidylinositol 3-kinase-Akt (PI3K/AKT), and estrogen receptor (ER) signaling pathways, respectively. Taken together, these observations suggest that βE2 exerts antioxidative effects following light-induced retinal degeneration potentially via NRF2 activation. This protective mechanism may depend on two pathways: a rapid, non-genomic-type PI3K/AKT response, and a genomic-type ER-dependent response. Our data provides evidence that βE2 is potentially effective for treatment of retinal degeneration diseases. | |||
| TO cite this article:ZHU Chunhui,LI Hongbo,WANG Shaolan, et al. 17β-Estradiol Up-Regulates NRF2 via PI3k/AKT and Estrogen Receptor Signaling Pathways to Suppress Light-Induced Retinal Degeneration in Rat[J]. | |||
| 5. Inhibition of GSK-3β activity decreases photoreceptor cell death in rat retina | |||
| Wang Baoying,Hu Chenghu,Feng Yan,Li Hongbo,Du Fangying,Zhu Chunhui,Yu Xiaorui | |||
| Basic Medicine 27 January 2015 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Photoreceptor cell death leading to retinal degeneration could be induced by physical or chemical treatments. However, the progress of photoreceptor cell death and underlying cellular and molecular mechanisms remain largely unexplored. Our previous studies have shown that Phosphatidylinositol-3-kinase (PI3K) signaling could mediate the effect of 17β-Estradiol (βE2) which protects photoreceptor cells from death. In present study, we report a novel finding that phosphorylation of glycogen synthase kinase-3β (GSK-3β) controlled by PI3K/Akt signaling is a potent mediator in photoreceptor cell death. In two different animal models of retinal degeneration, light-damaged or N-Methyl-N-nitrosourea (MNU)-induced, GSK-3β phosphorylation was inhibited. Furthermore, phosphorylating Ser9 of GSK-3β with Lithium chloride (LiCl) was able to protect photoreceptor cells, whereas inhibition of the PI3K/Akt with LY294002 which decreases GSK-3β phosphorylation could not protect retinal cells from death. Our results suggest GSK-3β activity is closely related to photoreceptor cell death, and the application of GSK-3β inhibitor LiCl can reduce photoreceptor cell death in retinal degeneration. | |||
| TO cite this article:Wang Baoying,Hu Chenghu,Feng Yan, et al. Inhibition of GSK-3β activity decreases photoreceptor cell death in rat retina[OL].[27 January 2015] http://en.paper.edu.cn/en_releasepaper/content/4630222 | |||
| 6. 17β-Estradiol Protects the Sprague-Dawley Rats Retinal from Light-Induced Damage via Anti-oxidation | |||
| Wang Shaolan,Wang Baoying,Feng Yan,Mo Mingshu,Du Fangying,Li Hongbo,Yu Xiaorui | |||
Basic Medicine 27 June 2014
|
|||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Oxidative stress is thought to be a major cause of light induced retinal neurodegeneration. The protective role of 17β-estradiol (βE2) in neurodegenerative disorders is well known, however, the underlying mechanism remains unclear. Here, we applied light induced retinal damage model to explore the mechanism by which βE2 exerts its neuroprotection. Adult male and female- ovariectomized (OVX) rats were exposed to 8000 lx white light for 12h to induce retinal light damage. Electroretinogram (ERG) assay and hematoxylin and eosin (H&E) staining show that exposure to light for 12h resulted in functional damage to the rat retina, histological changes and retinal neurons loss, while intravitreal injection (IVI) with βE2 significantly rescued impaired retina function in both female and male rats. By detecting malonylodialdehyde (MDA) production (a biomarker for oxidative stress) indicated an increasing retinal oxidative stress following exposure to light, and βE2 reduced the light induced oxidative stress. qRT-PCR indicated that antioxidant enzymes SOD and Gpx mRNA level were diminished in female-OVX rats but up-regulated in male rats after exposing to light, suggesting a gender differences in regulating the genes of these antioxidant enzymes in response to light. However, administration of βE2 recovered or enhanced the SOD and Gpx expression upon light stimulation. In spite of the CAT expression was not sensitive to light, βE2 also increased the gene expressions both in female-OVX and male rats. Further study indicated the antioxidant proteins Trx and Nrf2 were also involved in βE2 mediated anti-oxidation, while cytoprotective HO-1 exerts a key role in endogenous defense mechanisms against light but not via βE2. Taken together, we provide evidence that βE2 protected the retinal from light damage via anti-oxidative effect, the underline mechanism involved in regulation of the genes of antioxidant enzymes (SOD, CAT, Gpx) and proteins (Trx and Nrf2). Our study will provide the theory evidence for estrogen replacement therapy in postmenopausal women for reducing the risk of Age-related macular degeneration. | |||
| TO cite this article:Wang Shaolan,Wang Baoying,Feng Yan, et al. 17β-Estradiol Protects the Sprague-Dawley Rats Retinal from Light-Induced Damage via Anti-oxidation[OL].[27 June 2014] http://en.paper.edu.cn/en_releasepaper/content/4602681 | |||
| 7. Gene Expression Profile of Hedgehog Signaling Pathway Inhibition in Human Carcinoma Cells | |||
| TANG Xiaoli,DENG Libin,ZHANG Weilong,GAO Meng,HUANG Dengliang,LUO Shiwen,LU Quqin | |||
| Basic Medicine 10 March 2014
|
|||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Background: Aberrant activation of the Hedgehog (Hh) signaling pathway frequency occurs in human cancers, and increased evidence implicates the considerable role of GANT61 (Gli-ANTagonist, a kind of Hh signaling inhibitor) in anticancer therapy. However, it is still lacking the systematic scanning for the common mechanism of various cancer cells in respond to Hh-inhibition. Methodology/Principal Findings: Gene expression profiling of Hh inhibited HT-29 and MKN45 cells was determined by Illumina? Sentrix? BeadChip arrays. From the 17,329 expressed genes across genome, we identified 668 and 269 differentially expressed genes (DEGs, p < 0.01) in comparison pairs of HT-29 and MKN45, respectively. Interesting, large number of common DEGs (77 genes) were seen in both two comparison pairs, which was clearly more than the predicted number (10, p < 10?4). Further interpretation of gene ontology was based on over-representation analysis. Two nested categories of GO biological processes ("cell death", and "response to stimulus") were detected as candidates with the enrichments of DEGs in both two cell lines. In addition, cDNA microarray profiling of extra cancer cells (ES2 and H4) verified the change of expression in six common DEGs related to "cell death" (CDKN1A, DDIT3, IER3, IL8, MFGE8, and PPP1R15A) following GANT61 treatment. Conclusions/Significance: Our research indicates that inhibition of Hh has considerable effect on genes from pathway of "cell death" in various carcinoma cells. And, the aberrant of "response to DNA damage" related genes (such as DDIT3) may play a critical role in GANT61-induced cell death. In summary, this dataset provide insight into the molecular mechanisms of GANT61-induced antitumor activity, and the list of novel GLI-targets in cancer cells. | |||
| TO cite this article:TANG Xiaoli,DENG Libin,ZHANG Weilong, et al. Gene Expression Profile of Hedgehog Signaling Pathway Inhibition in Human Carcinoma Cells[OL].[10 March 2014] http://en.paper.edu.cn/en_releasepaper/content/4589220 | |||
| 8. Identification of β1,4-galactosyltransferase I As a target gene of Aflatoxin B1 | |||
| Jiang Jianhai,Wei Yuanyan,Gu Jianxin | |||
| Basic Medicine 03 January 2011 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Objective To investigae the effec of Aflatoxin B1 (AFB1) exposure, an etiological factors associated with hepatocellular carcinoma on the expression of β1,4-galactosyltransferase I. Methods Immunohistochemistry method was used to detect the expression of GalT I in hepatoma tissues and normal tissues. And, double luciferase reporter analysis was used to detect the effect of Aflatoxin B1 on GalT promoter activity. Results β1,4-galactosyltransferase I (GalT I) is significantly up-regulated in hepatoma, and is transcriptionally regulated by AFB1. The AFB1-induced GalT I transcription is mediacted by E2F1 transcription factor. Conclusions These results provide genetic evidence that GalT I upregulation mediated by E2F1 might contribute to hepatoma development mediated by AFB1. | |||
| TO cite this article:Jiang Jianhai,Wei Yuanyan,Gu Jianxin. Identification of β1,4-galactosyltransferase I As a target gene of Aflatoxin B1[OL].[ 3 January 2011] http://en.paper.edu.cn/en_releasepaper/content/4403552 | |||
| 9. Involvement of STAT5a signaling in morphine-induced up-regulation of the cyclin D1 | |||
| Liyuan Guo,Hui Li,Han Liu,Chaoying Li,Mengsen Li,Wei Jiang,Peng He,Shanshan Wang,Michael A McNutt,Gang Li | |||
| Basic Medicine 24 July 2009 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Opioids receptor and cytokine receptor has been verified to have a functional link and interaction. However, if opioid receptor in lymphocytes shares cytokine signal pathway is not well defined. The presented results from confocal microscopy and Western blotting showed that morphine treatment was able to activate cytoplasmic STAT5a in CEM x174 cells, which was then translocated into nuclei and bound to elements of cyclin D1 promoter, and as a consequence the expression of the cyclin D1 was apparently up-regulated. The data from EMSA-superEMSA and ChIP-qPCR further confirmed that morphine was capable of promoting the binding of STAT5a to its elements (proximal and distal), which was abolished by antagonist naloxone. As shown in transient transfection assay, activity of the cyclin D1 promoter was significantly reduced by 82% (distal) and 65% (proximal) in comparison with wild type after two STAT5a elements were mutated. Furthermore, knockdown of the STAT5a was associated with a concurrent silence of morphine-induced expression upregulation？ of the cyclin D1, indicating the involvement of STAT5a in morphine-triggered signaling in regulation of the cyclin D1 expression. The finding provides evidence which demonstrates the cross-talk between mu opioid receptor and cytokine signaling in lymphocytes. Thus, we conclude that morphine may modulate cyclin D1 gene expression via STATs signaling, which will be favorable for further understanding of the pharmacological effect of morphine on immune regulation. | |||
| TO cite this article:Liyuan Guo,Hui Li,Han Liu, et al. Involvement of STAT5a signaling in morphine-induced up-regulation of the cyclin D1[OL].[24 July 2009] http://en.paper.edu.cn/en_releasepaper/content/34079 | |||
| 10. The effect of acetylation of FoxO1 on activating Bim expression in response to HDAC inhibitor depsipeptide treatment | |||
| Yang Yang,Zhao Ying,Liao Wenjuan,Yang Jing,Zhu Weiguo | |||
| Basic Medicine 31 March 2009 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Histone deacetylase (HDAC) inhibitors have been shown to induce cell cycle arrest and apoptosis in cancer cells. However, the mechanisms of HDAC inhibitor induced apoptosis are incompletely understood. In previous study, we found that HDAC inhibitor depsipeptide may induce apoptosis of human lung cancer cells through the forkhead box class O1 (FoxO1)-Bim pathway. In this study, we further explore the mechanisms of mediating FoxO1 after depsipeptide treatment in lung cancer cells. We found that depsipeptide-induced expression of Bim was directly dependent on acetylation of FoxO1 that is catalyzed by cAMP-responsive element-binding protein (CREB)-binding protein (CBP). Moreover, our results demonstrated that FoxO1 acetylation is required for the depsipeptide induced activation of Bim and apoptosis, using transfection with a plasmid containing FoxO1 mutated at lysine sites. These data show for the first time that a HDAC inhibitor induces apoptosis through the FoxO1 acetylation-Bim pathway. | |||
| TO cite this article:Yang Yang,Zhao Ying,Liao Wenjuan, et al. The effect of acetylation of FoxO1 on activating Bim expression in response to HDAC inhibitor depsipeptide treatment[OL].[31 March 2009] http://en.paper.edu.cn/en_releasepaper/content/30933 | |||
| Select/Unselect all | For Selected Papers |
Saved Papers
Please enter a name for this paper to be shown in your personalized Saved Papers list
|
|
 |
|
||||||||||||||
About Sciencepaper Online |
Privacy Policy |
Terms & Conditions |
Contact Us
Technology Partner - CERNET