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Search Results: 1 - 10 of 23383 matches for " Dingbo Shi "
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Quercetin Suppresses Cyclooxygenase-2 Expression and Angiogenesis through Inactivation of P300 Signaling
Xiangsheng Xiao,Dingbo Shi,Liqun Liu,Jingshu Wang,Xiaoming Xie,Tiebang Kang,Wuguo Deng
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0022934
Abstract: Quercetin, a polyphenolic bioflavonoid, possesses multiple pharmacological actions including anti-inflammatory and antitumor properties. However, the precise action mechanisms of quercetin remain unclear. Here, we reported the regulatory actions of quercetin on cyclooxygenase-2 (COX-2), an important mediator in inflammation and tumor promotion, and revealed the underlying mechanisms. Quercetin significantly suppressed COX-2 mRNA and protein expression and prostaglandin (PG) E(2) production, as well as COX-2 promoter activation in breast cancer cells. Quercetin also significantly inhibited COX-2-mediated angiogenesis in human endothelial cells in a dose-dependent manner. The in vitro streptavidin-agarose pulldown assay and in vivo chromatin immunoprecipitation assay showed that quercetin considerably inhibited the binding of the transactivators CREB2, C-Jun, C/EBPβ and NF-κB and blocked the recruitment of the coactivator p300 to COX-2 promoter. Moreover, quercetin effectively inhibited p300 histone acetyltransferase (HAT) activity, thereby attenuating the p300-mediated acetylation of NF-κB. Treatment of cells with p300 HAT inhibitor roscovitine was as effective as quercetin at inhibiting p300 HAT activity. Addition of quercetin to roscovitine-treated cells did not change the roscovitine-induced inhibition of p300 HAT activity. Conversely, gene delivery of constitutively active p300 significantly reversed the quercetin-mediated inhibition of endogenous HAT activity. These results indicate that quercetin suppresses COX-2 expression by inhibiting the p300 signaling and blocking the binding of multiple transactivators to COX-2 promoter. Our findings therefore reveal a novel mechanism of action of quercetin and suggest a potential use for quercetin in the treatment of COX-2-mediated diseases such as breast cancers.
Nicotine Promotes Proliferation of Human Nasopharyngeal Carcinoma Cells by Regulating α7AChR, ERK, HIF-1α and VEGF/PEDF Signaling
Dingbo Shi, Wei Guo, Wangbin Chen, Lingyi Fu, Jingshu Wang, Yung Tian, Xiangsheng Xiao, Tiebang Kang, Wenlin Huang, Wuguo Deng
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0043898
Abstract: Nicotine, the major component in cigarette smoke, can promote tumor growth and angiogenesis, but the precise mechanisms involved remain largely unknown. Here, we investigated the mechanism of action of nicotine in human nasopharyngeal carcinoma (NPC) cells. Nicotine significantly promoted cell proliferation in a dose and time-dependent manner in human NPC cells. The mechanism studies showed that the observed stimulation of proliferation was accompanied by the nicotine-mediated simultaneous modulation of α7AChR, HIF-1α, ERK and VEGF/PEDF signaling. Treatment of NPC cells with nicotine markedly upregulated the expression of α7AChR and HIF-1α proteins. Transfection with a α7AChR or HIF-1α-specific siRNA or a α7AChR-selective inhibitor significantly attenuated the nicotine-mediated promotion of NPC cell proliferation. Nicotine also promoted the phosphorylation of ERK1/2 but not JNK and p38 proteins, thereby induced the activation of ERK/MAPK signaling pathway. Pretreatment with an ERK-selective inhibitor effectively reduced the nicotine-induced proliferation of NPC cells. Moreover, nicotine upregulated the expression of VEGF but suppressed the expression of PEDF at mRNA and protein levels, leading to a significant increase of the ratio of VEGF/PEDF in NPC cells. Pretreatment with a α7AChR or ERK-selective inhibitor or transfection with a HIF-1α-specific siRNA in NPC cells significantly inhibited the nicotine-induced HIF-1α expression and VEGF/PEDF ratio. These results therefore indicate that nicotine promotes proliferation of human NPC cells in vitro through simultaneous modulation of α7AChR, HIF-1α, ERK and VEGF/PEDF signaling and suggest that the related molecules such as HIF-1α might be the potential therapeutic targets for tobacco-associated diseases such as nasopharyngeal carcinomas.
Lasiodin Inhibits Proliferation of Human Nasopharyngeal Carcinoma Cells by Simultaneous Modulation of the Apaf-1/Caspase, AKT/MAPK and COX-2/NF-κB Signaling Pathways
Lianzhu Lin, Wuguo Deng, Yun Tian, Wangbing Chen, Jingshu Wang, Lingyi Fu, Dingbo Shi, Mouming Zhao, Wei Luo
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0097799
Abstract: Rabdosia serra has been widely used for the treatment of the various human diseases. However, the antiproliferative effects and underlying mechanisms of the compounds in this herb remain largely unknown. In this study, an antiproliferative compound against human nasopharyngeal carcinoma (NPC) cells from Rabdosia serra was purified and identified as lasiodin (a diterpenoid). The treatment with lasiodin inhibited cell viability and migration. Lasiodin also mediated the cell morphology change and induced apoptosis in NPC cells. The treatment with lasiodin induced the Apaf-1 expression, triggered the cytochrome-C release, and stimulated the PARP, caspase-3 and caspase-9 cleavages, thereby activating the apoptotic pathways. The treatment with lasiodin also significantly inhibited the phosphorylations of the AKT, ERK1/2, p38 and JNK proteins. The pretreatment with the AKT or MAPK-selective inhibitors considerably blocked the lasiodin-mediated inhibition of cell proliferation. Moreover, the treatment with lasiodin inhibited the COX-2 expression, abrogated NF-κB binding to the COX-2 promoter, and promoted the NF-κB translocation from cell nuclei to cytosol. The pretreatment with a COX-2-selective inhibitor abrogated the lasiodin-induced inhibition of cell proliferation. These results indicated that lasiodin simultaneously activated the Apaf-1/caspase-dependent apoptotic pathways and suppressed the AKT/MAPK and COX-2/NF-κB signaling pathways. This study also suggested that lasiodin could be a promising natural compound for the prevention and treatment of NPC.
Determination of the geopotential and orthometric height based on frequency shift equation  [PDF]
Wenbin Shen, Jinsheng Ning, Jingnan Liu, Jiancheng Li, Dingbo Chao
Natural Science (NS) , 2011, DOI: 10.4236/ns.2011.35052
Abstract: The orthometric height (OH) system plays a key role in geodesy, and it has broad applications in various fields and activities. Based on general relativity theory (GRT), on an arbitrary equi-geo- potential surface, there does not exist the gravity frequency shift of an electromagnetic wave signal. However, between arbitrary two different equi-geopotential surfaces, there exists the gra- vity frequency shift of the signal. The relationship between the geopotential difference and the gravity frequency shift between arbitrary two points P and Q is referred to as the gravity frequency shift equation. Based on this equation, one can determine the geopotential difference as well as the OH difference between two separated points P and Q either by using electromagnetic wave signals propagated between P and Q, or by using the Global Positioning System (GPS) satellite signals received simultaneously by receivers at P and Q. Suppose an emitter at P emits a signal with frequency f towards a receiver at Q, and the received frequency of the signal at Q is , or suppose an emitter on board a flying GPS satellite emits signals with frequency f towards two receivers at P and Q on ground, and the received frequencies of the signals at P and Q are and , respectively, then, the geopoten-tial dif- ference between these two points can be determined based on the geopotential frequen- cy shift equation, using either the gravity frequency shift ? f or ? , and the corresponding OH difference is further determined based on the Bruns’ formula. Besides, using this approach a unified world height datum system might be realized, because P and Q could be chosen quite arbitrarily, e.g., they are located on two separated continents or islands.
Ursolic Acid Simultaneously Targets Multiple Signaling Pathways to Suppress Proliferation and Induce Apoptosis in Colon Cancer Cells
Jingshu Wang, Liqun Liu, Huijuan Qiu, Xiaohong Zhang, Wei Guo, Wangbing Chen, Yun Tian, Lingyi Fu, Dingbo Shi, Jianding Cheng, Wenlin Huang, Wuguo Deng
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0063872
Abstract: Ursolic acid (UA), a natural pentacyclic triterpenoid carboxylic acid distributed in medical herbs, exerts antitumor effects and is emerging as a promising compound for cancer prevention and therapy, but its excise mechanisms of action in colon cancer cells remains largely unknown. Here, we identified the molecular mechanisms by which UA inhibited cell proliferation and induced apoptosis in human colon cancer SW480 and LoVo cells. Treatment with UA led to significant inhibitions in cell viability and clone formation and changes in cell morphology and spreading. UA also suppressed colon cancer cell migration by inhibiting MMP9 and upregulating CDH1 expression. Further studies showed that UA inhibited the phosphorylation of Akt and ERK proteins. Pretreatment with an Akt or ERK-specific inhibitor considerably abrogated the proliferation inhibition by UA. UA also significantly inhibited colon cancer cell COX-2 expression and PGE2 production. Pretreatment with a COX-2 inhibitor (celecoxib) abrogated the UA-induced cell proliferation. Moreover, we found that UA effectively promoted NF-κB and p300 translocation from cell nuclei to cytoplasm, and attenuated the p300-mediated acetylation of NF-κB and CREB2. Pretreatment with a p300 inhibitor (roscovitine) abrogated the UA-induced cell proliferation, which is reversed by p300 overexpression. Furthermore, UA treatment induced colon cancer cell apoptosis, increased the cleavage of PARP, caspase-3 and 9, and trigged the release of cytochrome c from mitochondrial inter-membrane space into cytosol. These results indicate that UA inhibits cell proliferation and induces apoptosis in colon cancer cells through simultaneous modulation of the multiple signaling pathways such as MMP9/CDH1, Akt/ERK, COX-2/PGE2, p300/NF-κB/CREB2, and cytochrome c/caspase pathways.
Upregulation of Cleavage and Polyadenylation Specific Factor 4 in Lung Adenocarcinoma and Its Critical Role for Cancer Cell Survival and Proliferation
Wangbing Chen, Wei Guo, Mei Li, Dingbo Shi, Yun Tian, Zhenlin Li, Jingshu Wang, Lingyi Fu, Xiangsheng Xiao, Quentin Qiang Liu, Shusen Wang, Wenlin Huang, Wuguo Deng
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0082728
Abstract: Cleavage and polyadenylation specific factor 4 (CPSF4), a member of CPSF complex, plays a key role in mRNA polyadenylation and mRNA 3′ ends maturation. However, its possible role in lung cancer pathogenesis is unknown. In this study, we investigated the biological role and clinical significance of CPSF4 in lung cancer growth and survival and elucidated its underlying molecular mechanisms. We found that CPSF4 was highly expressed in lung adenocarcinoma cell lines and tumor tissue but was undetectable in 8 normal human tissues. We also found that CPSF4 overexpression was correlated with poor overall survival in patients with lung adenocarcinomas (P<0.001). Multivariate survival analyses revealed that higher CPSF4 expression was an independent prognostic factor for overall survival of the patients with lung adenocarcinomas. Suppression of CPSF4 by siRNA inhibited lung cancer cells proliferation, colony formation, and induced apoptosis. Mechanism studies revealed that these effects were achieved through simultaneous modulation of multiple signaling pathways. Knockdown of CPSF4 expression by siRNA markedly inhibited the phosphorylation of PI3K, AKT and ERK1/2 and JNK proteins. In contrast, the ectopic expression of CPSF4 had the opposite effects. Moreover, CPSF4 knockdown also induced the cleavage of caspase-3 and caspse-9 proteins. Collectively, these results demonstrate that CPSF4 plays a critical role in regulating lung cancer cell proliferation and survival and may be a potential prognostic biomarker and therapeutic target for lung adenocarcinoma.
Berberine Targets AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF and Cytochrome-c/Caspase Signaling to Suppress Human Cancer Cell Growth
Lingyi Fu, Wangbing Chen, Wei Guo, Jingshu Wang, Yun Tian, Dingbo Shi, Xiaohong Zhang, Huijuan Qiu, Xiangsheng Xiao, Tiebang Kang, Wenlin Huang, Shusen Wang, Wuguo Deng
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0069240
Abstract: Berberine (BBR), an isoquinoline derivative alkaloid isolated from Chinese herbs, has a long history of uses for the treatment of multiple diseases, including cancers. However, the precise mechanisms of actions of BBR in human lung cancer cells remain unclear. In this study, we investigated the molecular mechanisms by which BBR inhibits cell growth in human non-small-cell lung cancer (NSCLC) cells. Treatment with BBR promoted cell morphology change, inhibited cell migration, proliferation and colony formation, and induced cell apoptosis. Further molecular mechanism study showed that BBR simultaneously targeted multiple cell signaling pathways to inhibit NSCLC cell growth. Treatment with BBR inhibited AP-2α and AP-2β expression and abrogated their binding on hTERT promoters, thereby inhibiting hTERT expression. Knockdown of AP-2α and AP-2β by siRNA considerably augmented the BBR-mediated inhibition of cell growth. BBR also suppressed the nuclear translocation of p50/p65 NF-κB proteins and their binding to COX-2 promoter, causing inhibition of COX-2. BBR also downregulated HIF-1α and VEGF expression and inhibited Akt and ERK phosphorylation. Knockdown of HIF-1α by siRNA considerably augmented the BBR-mediated inhibition of cell growth. Moreover, BBR treatment triggered cytochrome-c release from mitochondrial inter-membrane space into cytosol, promoted cleavage of caspase and PARP, and affected expression of BAX and Bcl-2, thereby activating apoptotic pathway. Taken together, these results demonstrated that BBR inhibited NSCLC cell growth by simultaneously targeting AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF, PI3K/AKT, Raf/MEK/ERK and cytochrome-c/caspase signaling pathways. Our findings provide new insights into understanding the anticancer mechanisms of BBR in human lung cancer therapy.
Detection of unsymmetrical global tectonic change by using space geodetic data

SUN FupingZHAO MingNING Jinsheng CHAO Dingbo,

科学通报(英文版) , 2000,
Abstract: The global tectonic change deduced from geophysical research was first identified by space geodetic data from VLBI, GPS and SLR measurements. Whether using geodesic rates or using vertical velocities of stations, three kinds of data and their integration give consistent results: within the mid-latitude belt on the Northern Hemisphere there may be about 8–10 mm/a contracting change; within the mid-latitude belt on the Southern Hemisphere there may be about 12–14 mm/a expanding change. This result not only validates the reverse global tectonic change in the Southern and Northern Hemispheres of the Earth, but also gives relatively precise quantative estimations.
Detection of unsymmetrical global tectonic change by using space geodetic data
Fuping Sun,Ming Zhao,Jinsheng Ning,Dingbo Chao
Chinese Science Bulletin , 2000, DOI: 10.1007/BF02886042
Abstract: The global tectonic change deduced from geophysical research was first identified by space geodetic data from VLBI, GPS and SLR measurements. Whether using geodesic rates or using vertical velocities of stations, three kinds of data and their integration give consistent results: within the mid-latitude belt on the Northern Hemisphere there may be about 8–10 mm/a contracting change; within the mid-latitude belt on the Southern Hemisphere there may be about 12–14 mm/a expanding change. This result not only validates the reverse global tectonic change in the Southern and Northern Hemispheres of the Earth, but also gives relatively precise quantative estimations.
COMPARISON OF DIFFERENT SPECTRAL MATCH MODELS
地物光谱匹配模型比较研究

Xu WeiDong,Yin Qiu,Kuang DingBo,
许卫东
,尹球,匡定波

红外与毫米波学报 , 2005,
Abstract: Tree spectral match models including minimums distance (MD), spectral angel model (SAM), spectral correlation fitting (SCF), were calculated and analyzed based on the spectrums taken from the field. However, the difference of the three models is not significant. The SAM was better but far from the best. Under this circumstance, derivative method was used to enhance the ability of discrimination. The match models were recalculated after the first derivative. Better results are achieved and the discriminability is remarkably enhanced, especially to the minimums distance model.
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