|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | miR-129-2 suppresses proliferation and migration of esophageal carcinomacells through downregulation of SOX4 expression显示文摘 | Min Kang Yumei Li Wenqi Liu Rensheng Wang Anzhou Tang Hong Hao Zhenguo Liu Hesheng Ou | 2013 | International Journal of Molecular Medicine2013，，1： | 1 |
| 2 | Effect Evaluation and Intelligent Prediction of Power Substation Project Considering New Energy显示文摘The evaluation of the implementation effect of the power substation project can find out the problems of the project more comprehensively,which has important practical significance for the further development of the power substation project.To ensure accuracy and real-time evaluation,this paper proposes a novel hybrid intelligent evaluation and prediction model based on improved TOPSIS and Long Short-Term Memory(LSTM)optimized by a Sperm Whale Algorithm(SWA).Firstly,under the background of considering the development of new energy,the influencing factors of power substation project implementation effect are analyzed from three aspects of technology,economy and society.Moreover,an evaluation model based on improved TOPSIS is constructed.Then,an intelligent prediction model based on SWA optimized LSTM is designed.Finally,the scientificity and accuracy of the proposed model are verified by empirical analysis,and the important factors affecting the implementation effect of power substation projects are pointed out. | Huiying Wu Meihua Zou Ye Ke Wenqi Ou Yonghong Li Minquan Ye | 2022 | Computer Modeling in Engineering & Sciences2022，，9： | 1 |
| 3 | Anti-tumor activities and apoptotic mechanism of ribosome-inactivating proteins显示文摘Ribosome-inactivating proteins(RIPs) belong to a family of enzymes that attack eukaryotic ribosomes and potently inhibit cellular protein synthesis.RIPs possess several biomedical properties,including anti-viral and anti-tumor activities.Multiple RIPs are known to inhibit tumor cell proliferation through inducing apoptosis in a variety of cancers,such as breast cancer,leukemia/lymphoma,and hepatoma.This review focuses on the anti-tumor activities of RIPs and their apoptotic effects through three closely related pathways:mitochondrial,death receptor,and endoplasmic reticulum pathways. | Meiqi Zeng Manyin Zheng Desheng Lu Jun Wang Wenqi Jiang Ou Sha | 2015 | Chinese Journal of Cancer2015，34，8： | 1 |
| 4 | SIRT2 interacts with DDX24 to promote nasopharyngeal carcinoma growth显示文摘Background:Nasopharyngeal carcinoma(NPC)is one of the most prevalent cancers in Southeast Asia.Sirtuin 2(SIRT2)is a member of the NAD+-dependent deacetylase family and has been shown to play important roles in numerous biological processes.However,Its function in NPC remains uncertain.The primary aim of this study is to clarify the role of SIRT2 in NPC.Methods:In this research,we examined the effect of SIRT2 silencing on NPC cell proliferation and colony formation using vitro NPC cell lines.Co-immunoprecipitation and mass spectrometry was applied to identify SIRT2-interacting proteins in NPC cells.Results:In comparison to nasopharyngeal epithelial NP69 cells,SIRT2 was up-regulated in multiple NPC cell lines,particularly in CNE2 cells.SIRT2 knockdown abrogated CNE2 cell proliferation and colony formation,whereas SIRT2 overexpression promoted HNE1 cell proliferation and colony formation.The SIRT2-interacting proteins were gathered in gene expression and regulation processes including RNA processing and translation.Among the SIRT2-interacting proteins,there were multiple DEAD-box(DDX)family members.Of note,silencing of DDX24 phenocopied the effect of SIRT2 knockdown on NPC growth.Overexpression of DDX24 restored SIRT2-depleted CNE2 cells to proliferative and colony formation.Conclusions:Our study indicates that SIRT2 can interact with DDX24 to enhance NPC growth.The clinical relevance of SIRT2 and DDX24 in NPC warrants further investigation. | HAIYING YUE CHUNHUI WANG HUIJUN ZHU QINGHUA DU JIAN LI XUE OU XIANGDE LI QIULU ZHONG YITING XIE DANJING LUO YIHE LI CHUNXIAO LIANG XUEMEI XU SONGNAN DU WENQI LIU | 2023 | BIOCELL2023，47，11： | 0 |
| 5 | Ginsenoside-Rg1 combined with a conditioned medium from induced neuron-like hUCMSCs alleviated the apoptosis in a cell model of ALS through regulating the NF-κB/Bcl-2 pathway显示文摘Amyotrophic lateral sclerosis(ALS)is a fatal neurodegenerative disease affecting both upper and lower motor neurons in the brain and spinal cord.One important aspect of ALS pathogenesis is superoxide dismutase 1(SOD1)mutant-mediated mitochondrial toxicity,leading to apoptosis in neurons.This study aimed to evaluate the neural protective synergistic effects of ginsenosides Rg1(G-Rg1)and conditioned medium(CM)on a mutational SOD1 cell model,and to explore the underlying mechanisms.We found that the contents of nerve growth factor,glial cell line-derived neurotrophic factor,and brain-derived neurotrophic factor significantly increased in CM after human umbilical cord mesenchymal stem cells(hUCMSCs)were exposed to neuron differentiation reagents for seven days.CM or G-Rg1 decreased the apoptotic rate of SOD1^(G93A)-NSC34 cell to a certain extent,but their combination brought about the least apoptosis,compared with CM or G-Rg1 alone.Further research showed that the anti-apoptotic protein Bcl-2 was upregulated in all the treatment groups.Proteins associated with mitochondrial apoptotic pathways,such as Bax,caspase 9(Cas-9),and cytochrome c(Cyt c),were downregulated.Furthermore,CM or G-Rg1 also inhibited the activation of the nuclear factor-kappa B(NF-κB)signaling pathway by reducing the phosphorylation of p65 and IκBa.CM/G-Rg1 or their combination also reduced the apoptotic rate induced by betulinic acid(BetA),an agonist of the NF-κB signaling pathway.In summary,the combination of CM and G-Rg1 effectively reduced the apoptosis of SOD1^(G93A)-NSC34 cells through suppresing the NF-κB/Bcl-2 sgaling pathway(Fig.1 is a graphcal representation of the abstract). | HUANG Yu YANG Hui YANG Biying ZHENG Yu H OU Xiaomei CHEN Guiling ZHANG Wenqi ZENG Xiang DU Baoxin | 2023 | Chinese Journal of Natural Medicines2023，21，7： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员