Institution
Dalian Medical University
Education•Dalian, China•
About: Dalian Medical University is a education organization based out in Dalian, China. It is known for research contribution in the topics: Cancer & Apoptosis. The organization has 15623 authors who have published 9993 publications receiving 164145 citations.
Topics: Cancer, Apoptosis, Cell growth, Metastasis, PI3K/AKT/mTOR pathway
Papers published on a yearly basis
Papers
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TL;DR: This is the first time to report the significant hepatoprotective effect of TFs from R. laevigata Michx fruit against CCl4-induced liver injury in mice and the action should be through reducing oxidative stress and suppressing inflammation and apoptosis.
90 citations
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Sichuan University1, Guangzhou University2, Bengbu Medical College3, Fudan University4, Peking Union Medical College5, Sun Yat-sen University6, Harbin Medical University7, Shantou University8, Guangzhou Medical University9, Zhejiang University10, Capital Medical University11, Third Military Medical University12, Qingdao University13, Hebei Medical University14, Chinese PLA General Hospital15, China Medical University (PRC)16, Dalian Medical University17
TL;DR: The AHELP trial as discussed by the authors evaluated the efficacy and safety of apatinib in patients with pretreated advanced hepatocellular carcinoma, and showed that the drug significantly improved overall survival compared with placebo, with a manageable safety profile.
90 citations
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TL;DR: SCN has the potential to be an effective and safer nano-carrier for targeted delivery of therapeutic agents to tumors with elevated expression of tenascin-C in their microenvironment and a reduction in the accumulation of DOX in the drug's principal toxicity organs achieved by SCN-DOX led to the diminished systemic toxicity.
Abstract: As a glycosphingolipid that can bind to several extracellular matrix proteins, sulfatide has the potential to become an effective targeting agent for tumors overexpressing tenasin-C in their microenvironment. To overcome the dose-limiting toxicity of doxorubicin (DOX), a sulfatide-containing nanoliposome (SCN) encapsulation approach was employed to improve treatment efficacy and reduce side effects of free DOX. This study analysed in vitro characteristics of sulfatidecontaining nanoliposomal DOX (SCN-DOX) and assessed its cytotoxicity in vitro, as well as biodistribution, therapeutic efficacy, and systemic toxicity in a human glioblastoma U-118MG xenograft model. SCN-DOX was shown to achieve highest drug to lipid ratio (0.5:1) and a remarkable in vitro stability. Moreover, DOX encapsulated in SCN was shown to be delivered into the nuclei and displayed prolonged retention over free DOX in U-118MG cells. This simple two-lipid SCN-DOX nanodrug has favourable pharmacokinetic attributes in terms of prolonged circulation time, reduced volume of distribution and enhanced bioavailability in healthy rats. As a result of the improved biodistribution, an enhanced treatment efficacy of SCNDOX was found in glioma-bearing mice compared to the free drug. Finally, a reduction in the accumulation of DOX in the drug’s principal toxicity organs achieved by SCN-DOX led to the diminished systemic toxicity as evident from the plasma biochemical analyses. Thus, SCN has the potential to be an effective and safer nano-carrier for targeted delivery of therapeutic agents to tumors with elevated expression of tenascin-C in their microenvironment.
90 citations
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TL;DR: Investigating the molecular mechanisms by which BBR inhibits cell growth in human non-small-cell lung cancer (NSCLC) cells 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.
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.
90 citations
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TL;DR: The mechanisms of the ameliorating effects of dioscin against CCl(4) induced acute liver damage are investigated in this article. But, the results showed that Dioscin significantly inhibited (p < 0.01) the increases of serum ALT and AST activities compared with the CCl (4)-treated animals.
90 citations
Authors
Showing all 15657 results
Name | H-index | Papers | Citations |
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Jing Wang | 184 | 4046 | 202769 |
Jan-Åke Gustafsson | 147 | 1058 | 98804 |
Melitta Schachner | 135 | 861 | 67304 |
Yan Zhang | 107 | 2410 | 57758 |
Jau-Shyong Hong | 93 | 474 | 37172 |
Li Zhang | 92 | 918 | 35648 |
Charles G. Eberhart | 84 | 444 | 29920 |
Ying Lu | 83 | 343 | 24913 |
You-Lin Qiao | 78 | 595 | 23919 |
Wei Wei | 75 | 1068 | 29415 |
Weidong Le | 74 | 287 | 22551 |
Jin-Tai Yu | 66 | 439 | 20020 |
Wei Jiang | 65 | 660 | 18932 |
Lan Tan | 62 | 387 | 13828 |
Hua Li | 62 | 849 | 17933 |