Institution
Tianjin Medical University
Education•Tianjin, China•
About: Tianjin Medical University is a education organization based out in Tianjin, China. It is known for research contribution in the topics: Cancer & Metastasis. The organization has 19345 authors who have published 13942 publications receiving 241709 citations. The organization is also known as: Tiānjīn Yīkē Dàxué.
Topics: Cancer, Metastasis, Breast cancer, Population, Medicine
Papers published on a yearly basis
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TL;DR: Using a clonogenic coculture growth system and a xenograft mouse model, it is demonstrated that adhesion of mantle cell lymphoma and other non-Hodgkin lymphoma cells to lymphoma stromal cells confers drug resistance, clonogenicity, and induction of histone deacetylase 6 (HDAC6).
Abstract: A dynamic interaction occurs between the lymphoma cell and its microenvironment, with each profoundly influencing the behavior of the other. Here, using a clonogenic coculture growth system and a xenograft mouse model, we demonstrated that adhesion of mantle cell lymphoma (MCL) and other non-Hodgkin lymphoma cells to lymphoma stromal cells confers drug resistance, clonogenicity, and induction of histone deacetylase 6 (HDAC6). Furthermore, stroma triggered a c-Myc/miR-548m feed-forward loop, linking sustained c-Myc activation, miR-548m downregulation, and subsequent HDAC6 upregulation and stroma-mediated cell survival and lymphoma progression in lymphoma cell lines, primary MCL and other B cell lymphoma cell lines. Treatment with an HDAC6-selective inhibitor alone or in synergy with a c-Myc inhibitor enhanced cell death, abolished cell adhesion–mediated drug resistance, and suppressed clonogenicity and lymphoma growth ex vivo and in vivo. Together, these data suggest that the lymphoma-stroma interaction in the lymphoma microenvironment directly impacts the biology of lymphoma through genetic and epigenetic regulation, with HDAC6 and c-Myc as potential therapeutic targets.
66 citations
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TL;DR: The results support the use of the LEN and DEX combination as a new therapeutic regimen in clinical trials of MCL and delay the tumor growth and improved the survival of M CL-bearing mice.
66 citations
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TL;DR: Thalidomide inhibits vasculogenic mimicry channel and mosaic vessels formation in melanoma through the regulation of vasculogen factors, and it can induce necrosis of melanoma cells, which may be related with the NF-κB signaling pathway.
Abstract: To observe the effects of thalidomide on melanoma tumor growth and blood supply patterns in C57 mice. Thirty mice inoculated subcutaneously with B16F10 cells were randomly divided into the treatment group and the control group. Thalidomide was administered once a day at a dose of 200 mg/kg for the treatment group starting on the fifth day after inoculation, and an equivalent volume of 0.5% carboxylmethyl cellulose was administered similarly in the control group. The diameter of the tumors was measured daily after inoculation until the mice were sacrificed on the 19th day. The different blood supply patterns were counted after immunohistochemical and PAS histochemical double-Staining. VEGF, NF-κB, PCNA, MMP-2 and MMP-9 expression in tumor tissue was also assessed. The tumor volume(P = 0.019) and the number of vasculogenic mimicry(P = 0.03) and mosaic vessels(P = 0.004) in the treatment group were significantly decreased compared with the control group. VEGF(P = 0.004), NF-κB(P = 0.009), PCNA(P = 0.002), MMP-2 (P = 0.000), MMP-9(P = 0.002) protein expression and MMP-2(P = 0.000) and MMP-9(P = 0.000) mRNA in the treatment group were significantly lower than those in the control groups. Thalidomide inhibits vasculogenic mimicry channel and mosaic vessels formation in melanoma through the regulation of vasculogenic factors, and it can induce necrosis of melanoma cells, which may be related with the NF-κB signaling pathway.
66 citations
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TL;DR: It is found that at concentrations found in the ischemic brain, tPA interacts with synaptic but not extrasynaptic NMDARs, and Atf3 down-regulation abrogates the protective effect of tPA against excitotoxin-induced neuronal death.
66 citations
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TL;DR: Sanguinarine may be developed as an agent either alone or in combination with taxol for treatment of prostate cancer overexpressing survivin, offering a potential therapeutic strategy for overcoming taxol resistance.
Abstract: Prostate cancer is a frequently occurring disease and is the second leading cause of cancer-related deaths of men in the United States. Current treatments have proved inadequate in curing or controlling prostate cancer, and a search for agents for the management of this disease is urgently needed. Survivin plays an important role in both progression of castration-resistant prostate cancer and resistance to chemotherapy. Altered expression of survivin in prostate cancer cells is associated with cancer progression, drug/radiation resistance, poor prognosis, and short patient survival. In the present study, the authors performed a cell-based rapid screen of the Prestwick Chemical Library consisting of 1120 Food and Drug Administration-approved compounds with known safety and bioavailability in humans to identify potential inhibitors of survivin and anticancer agents for prostate cancer. Sanguinarine, a benzophenanthridine alkaloid derived primarily from the bloodroot plant, was identified as a novel inhibitor of survivin that selectively kills prostate cancer cells over "normal" prostate epithelial cells. The authors found that sanguinarine inhibits survivin protein expression through protein degradation via the ubiquitin-proteasome system. Sanguinarine induces apoptosis and inhibits growth of human prostate cancer cells and in vivo tumor formation. Administration of sanguinarine, beginning 3 days after ectopic implantation of DU145 human prostate cancer cells, reduces both tumor weight and volume. In addition, sanguinarine sensitized paclitaxel-mediated growth inhibition and apoptosis, offering a potential therapeutic strategy for overcoming taxol resistance. These results suggest that sanguinarine may be developed as an agent either alone or in combination with taxol for treatment of prostate cancer overexpressing survivin.
66 citations
Authors
Showing all 19408 results
Name | H-index | Papers | Citations |
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Yang Yang | 171 | 2644 | 153049 |
Wei Zheng | 151 | 1929 | 120209 |
Bo Wang | 119 | 2905 | 84863 |
Qian Wang | 108 | 2148 | 65557 |
Yongsheng Chen | 107 | 465 | 55962 |
Jian Zhang | 107 | 3064 | 69715 |
Wei Liu | 102 | 2927 | 65228 |
Bin Zhang | 99 | 435 | 55028 |
Lei Liu | 98 | 2041 | 51163 |
Chawnshang Chang | 97 | 534 | 35629 |
Bin Li | 92 | 1755 | 42835 |
Yihai Cao | 90 | 304 | 32712 |
Chen-Yu Zhang | 85 | 332 | 39724 |
Hsing Jien Kung | 85 | 349 | 30686 |
Susan K. Lutgendorf | 77 | 248 | 17318 |