31 research outputs found
Copper(I)-Mediated Cascade Reactions: An Efficient Approach to the Synthesis of Functionalized Benzofuro[3,2-<i>d</i>]pyrimidines
A novel cascade reaction was developed for the synthesis of diverse members of a series of benzofuro[3,2-<i>d</i>]pyrimidine derivatives. The process utilizes readily prepared 3-chlorochromenones and various commercially available amidines and their analogues as starting materials. This tandem reaction is promoted by using a simple copper(I) reagent and involves a chemoselective Michael addition–heterocyclization–intramolecular cyclization sequence
Supplementary_material – Supplemental material for CD44 overexpression related to lymph node metastasis and poor prognosis of pancreatic cancer
<p>Supplemental material, Supplementary_material for CD44 overexpression related to lymph node metastasis and poor prognosis of pancreatic cancer by Yijuan Liu, Ting Wu, Dong Lu, Jiantao Zhen and Lin Zhang in The International Journal of Biological Markers</p
Presentation1.PPT
<p>B4GALT5, also known as β-1, 4 galactosyltransferase V, is one of the members of β-1, 4 galactosyltransferase gene (B4GALT) family, which was concerned with embryonic development, tumor generation, other malignant diseases. In this study, we firstly cloned porcine B4GALT (pB4GALT5) from porcine alveolar macrophages, and predicted the structural domain and function of seven porcine β-1, 4 galactosyltransferase (I–VII) based on transcriptome analysis of PRRSV infected cells. Additionally, the upregulated porcine B4GALT5 expression was detected from PRRSV infected porcine alveolar macrophage (PAM) cells. The PRRSV proliferation were slightly inhibited in overexpression of pB4GALT5 transfected cells, the interaction of B4GALT5 and GP5 of PRRSV was firstly be detected by Co-IP, and the co-location between B4GALT5 and GP5 were also observed in golgi membranes by confocal microscopy. A significant increasing mRNA transcription, including inflammatory cytokines (IFN-α, IL-6, IL-18, IL-1β, TNF-α) and some cell surface glycosylated protein involved in antigen present (MHC-I/II), cell adhesion and migration (chemokine MCP-1 and receptor CCR2; LFA-1, ICAM-1) were upregulated in B4GALT5 overexpressed PRRSV infected cells. Our results demonstrated that the regulation of pB4GALT5 plays an important roles in PRRSV proliferation and modification function in viral infection cells. And these results will make achievements by supporting the research of latent mechanisms of β-1, 4 galactosyltransferase V in antiviral immunity.</p
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Mantle cell lymphoma (MCL) has a poor prognosis and high relapse rates despite current therapies, necessitating novel treatment regimens. Inhibition of SRC-3 show effectiveness in vivo and in vitro in other B cell lymphomas. Additionally, previous studies have shown that SRC-3 is highly expressed in the lymph nodes of B cell non-Hodgkin’s lymphoma patients, suggesting SRC-3 may play a role in the progression of B cell lymphoma. This study aimed to investigate novel SRC-3 inhibitors, SI-10 and SI-12, in mantle cell lymphoma. The cytotoxic effects of SI-10 and SI-12 were evaluated in vitro and demonstrated dose-dependent cytotoxicity in a panel of MCL cell lines. The in vivo efficacy of SI-10 was confirmed in two ibrutinib-resistant models: an immunocompetent disseminated A20 mouse model of B-cell lymphoma and a human PDX model of MCL. Notably, SI-10 treatment also resulted in a significant extension of survival in vivo with low toxicity in both ibrutinib-resistant murine models. We have investigated SI-10 as a novel anti-lymphoma compound via the inhibition of SRC-3 activity. These findings indicate that targeting SRC-3 should be investigated in combination with current clinical therapeutics as a novel strategy to expand the therapeutic index and to improve lymphoma outcomes.</div
Mino parental and Mino venetoclax resistant cells were treated with various concentrations of venetoclax.
B) Jeko-1 parental and Jeko-1 ibrutinib resistant cells were treated with ibrutinib at various concentrations. C) Mino parental and resistant cells were treated with SI-10 and SI-12. D) Jeko-1 parental and resistant cells were treated with SI-10 and SI-12.</p
MCL cell lines were treated with SRC-3 inhibitors.
A) SI-10 or B) SI-12 at various concentrations for 48 h and cell viability was determined using the resazurin assay C) Mino D) Jeko-1 growth inhibition with SI-10 (0–1 mM) for 6,12,24, or 48h.</p
SRC-3 treatment prolonged survival of A20-Balb/c mice.
Balb/c mice were injected with 1 x 106 A20 cells intravenously. Treatment started on day 7. A) Kaplan-Meier survival plot reflecting time to lethal tumor burden. Based on the log-rank test, there are significant differences between the treated group and the control (P < 0.05). B) Body weight of all groups were measured 5 days a week.</p
SRC-3 inhibitor treatment in normal mice show little to no toxicity after treatment for 28 days.
A) Body weight of all groups were measured 5 days a week. B) Blood serum levels of clinical markers related to kidney and liver failure. Dotted lines represent upper and lower limits based on reference values. Data outliers were removed using the identify outlier function in Graphpad Prism with the ROUT method (Q = 1%).</p
SRC-3 treatment decreased tumor growth in a Jeko-1 ibrutinib resistant mouse model.
A) Volumes of tumors treated with SI-10 (50 mg/kg), ibrutinib (100mg/kg) or vehicle B) Weight of tumors treated with SI-10 (50 mg/kg), ibrutinib (100mg/kg) or vehicle before sacrificing C) The weight of each mouse was measured 3 times a week.</p
Relative amount of DES in the progenies and in the control group under HL exposure.
<p>The concentrations of Vx, Ax and Zx were measured by HPLC. <i>DES</i> = (<i>Zx</i>+0.5<i>Ax</i>)/(<i>Vx</i>+<i>Ax</i>+<i>Zx</i>). The five progenies and the control group were grown under HL exposure (300–400 μmol photons m<sup>-2</sup> s<sup>-1</sup>) for 96 h. Each experimental HL exposure value was compared with the value found under normal conditions (0 h). n = 3+SD.</p