Publications by authors named "Yongtian Zhang"

5 Publications

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Long non-coding RNA TUG1 knockdown hinders the tumorigenesis of multiple myeloma by regulating the microRNA-34a-5p/NOTCH1 signaling pathway.

Open Life Sci 2020 9;15(1):284-295. Epub 2020 Jun 9.

Department of Hematology, Ji'ning No. 1 People's Hospital, Ji'ning, Shandong, China.

Multiple myeloma (MM) is a serious health issue in hematological malignancies. Long non-coding RNA taurine-upregulated gene 1 (TUG1) has been reported to be highly expressed in the plasma of MM patients. However, the functions of TUG1 in MM tumorigenesis along with related molecular basis are still undefined. In this study, increased TUG1 and decreased microRNA-34a-5p (miR-34a-5p) levels in MM tissues and cells were measured by the real-time quantitative polymerase reaction assay. The expression of relative proteins was determined by the Western blot assay. TUG1 knockdown suppressed cell viability, induced cell cycle arrest and cell apoptosis in MM cells, as shown by Cell Counting Kit-8 and flow cytometry assays. Bioinformatics analysis, luciferase reporter assay, and RNA pull-down assay indicated that miR-34a-5p was a target of TUG1 and directly bound to notch receptor 1 (NOTCH1), and TUG1 regulated the NOTCH1 expression by targeting miR-34a-5p. The functions of miR-34a-5p were abrogated by TUG1 upregulation. Moreover, TUG1 loss impeded MM xenograft tumor growth by upregulating miR-34a-5p and downregulating NOTCH1. Furthermore, TUG1 depletion inhibited the expression of Hes-1, Survivin, and Bcl-2 protein in MM cells and xenograft tumors. TUG1 knockdown inhibited MM tumorigenesis by regulating the miR-34a-5p/NOTCH1 signaling pathway and , deepening our understanding of the TUG1 function in MM.
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http://dx.doi.org/10.1515/biol-2020-0025DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7874539PMC
June 2020

Chitosan oligosaccharides prevent doxorubicin-induced oxidative stress and cardiac apoptosis through activating p38 and JNK MAPK mediated Nrf2/ARE pathway.

Chem Biol Interact 2019 May 28;305:54-65. Epub 2019 Mar 28.

Experimental and Teaching Center of Medical Basis for Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu, China. Electronic address:

Doxorubicin (DOX) is one of the most effective chemotherapeutic drugs; however, the incidence of cardiotoxicity compromises its therapeutic index. Oxidative stress and apoptosis are believed to be involved in DOX-induced cardiotoxicity. Chitosan oligosaccharides (COS), the enzymatic hydrolysates of chitosan, have been reported to possess diverse biological activities including antioxidant and anti-apoptotic properties. The objective of the present study was to investigate the potential role of COS against DOX-induced cardiotoxicity, and the effects of COS on apoptosis and oxidative stress in rats and H9C2 cells. Furthermore, we also shed light on the involved pathways during the whole process. For this purpose, first, we demonstrated that COS exhibited a significant protective effect on cardiac tissue by not only inducing a decrease in body and heart growth but also ameliorated oxidative damage and ECG alterations in DOX-treated rats. Second, we found that COS reversed the decrease of cell viability induced by DOX, reduced the intracellular reactive oxygen species (ROS), increased the mitochondrial membrane potential (MMP) and Bcl-2/Bax ratio. COS treatment also results in reduced caspase-3 and caspase-9 expressions, and an increase in the phosphorylation of MAPKs (mitogen-activated protein kinases) in DOX-exposed H9C2 cells. Additionally, cellular homeostasis was re-established via stabilization of MAPK mediated nuclear factor erythroid 2-related factor 2/antioxidant-response element (Nrf2/ARE) signaling and transcription of downstream cytoprotective genes. In summary, these findings suggest that COS could be a potential candidate for the prevention and treatment of DOX-induced cardiotoxicity.
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http://dx.doi.org/10.1016/j.cbi.2019.03.027DOI Listing
May 2019

Aplastic anemia preceding acute lymphoblastic leukemia in an adult with FAT1 mutation.

Minerva Med 2019 12 4;110(6):593-594. Epub 2019 Mar 4.

Department of Hematopathology, First People's Hospital, Jining, Shandong, China -

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http://dx.doi.org/10.23736/S0026-4806.19.06013-0DOI Listing
December 2019

Tumor necrosis factor receptor 2 may promote the proliferation and drug resistance of Kapras299 and L428 lymphoma cells via the AKT and WNT/β-catenin signaling pathways.

Oncol Lett 2018 Jun 30;15(6):8847-8852. Epub 2018 Mar 30.

Department of Hematology, First People's Hospital of Jining City, Jining, Shandong 257335, P.R. China.

Circulating soluble tumor necrosis factor receptor 2 (sTNFR2) has been associated with a relatively poor prognosis in various types of lymphoma. However, the specific role of TNFR2 expression in lymphoma cells remains uncharacterized. In the present study, TNFR2 expression was quantified in the Hodgkin lymphoma cell line, L428, and the anaplastic large-cell lymphoma cell line, Karpas299, using RT-PCR and western blot analyses. Karpas299 cells exhibited higher TNFR2 expression than L428 cells. Proliferation and drug resistance experiments demonstrated that Karpas299 cells also possessed a greater proliferative ability and resistance to adriamycin (ADM) than L428 cells, with 50% inhibitory concentrations (IC) of 1.423±0.24 µmol/l for Karpas299 cells, compared with 0.728±0.15 µmol/l for L428 cells (P<0.05). The knockdown of TNFR2 in Karpas299 cells significantly reduced their proliferative ability; when treated with ADM, the cell inhibition rate increased from 49.34±5.42% to 74.13±6.81% (P<0.05). The upregulation of TNFR2 in L428 cells significantly increased their proliferative ability; when treated with ADM, the cell inhibition rate decreased from 47.03±5.25% to 28.71±4.90% (P<0.05). Investigation of the underlying molecular mechanism indicated that the upregulation of TNFR2 expression in L428 cells increased the expression of β-catenin and the phosphorylation of AKT. In L428 cells overexpressing TNFR2, the β-catenin blocker, DKK1, or the AKT inhibitor, LY294002, abrogated the increase in proliferation induced by TNFR2 and increased cell inhibition rate upon treatment with ADM. In summary, the present study demonstrated that TNFR2 promoted the proliferative and drug resistance abilities of lymphoma cells via the AKT and WNT/β-catenin signaling pathways. This may provide the experimental basis for the further study of TNFR2 activity in lymphoma cells and warrant its investigation as a therapeutic target for lymphoma.
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http://dx.doi.org/10.3892/ol.2018.8396DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6004681PMC
June 2018

Clematichinenoside inhibits VCAM-1 and ICAM-1 expression in TNF-α-treated endothelial cells via NADPH oxidase-dependent IκB kinase/NF-κB pathway.

Free Radic Biol Med 2015 Jan 13;78:190-201. Epub 2014 Nov 13.

Department of Physiology, China Pharmaceutical University, Nanjing, Jiangsu, China. Electronic address:

Proinflammatory cytokine TNF-α-induced adhesion of leukocytes to endothelial cells plays a critical role in the early stage of atherosclerosis. Oxidative stress and redox-sensitive transcription factors are implicated in the process. Thus, compounds that mediate intracellular redox status and regulate transcription factors are of great therapeutic interest. Clematichinenoside (AR), a triterpene saponin isolated from the root of Clematis chinensis Osbeck, was previously demonstrated to have anti-inflammatory and antioxidative properties. However, little is known about the exact mechanism underlying these actions. Thus we performed a detailed study on its effect on leukocytes-endothelial cells adhesion with TNF-α-stimulated human umbilical vein endothelial cells (HUVECs) and cell-free systems. First, we found that AR reduced TNF-α-induced VCAM-1 and ICAM-1 expression and their promoter activity, inhibited translocation of p65 and phosphorylation of IκBα, suppressed IκB kinase-β (IKK-β) activity, lowered O2(∙-) and H2O2 levels, tackled p47(phox) translocation, and decreased NOX4 NADPH oxidase expression. Second, we showed that AR exhibited no direct free radical scavenging ability in cell-free systems at concentrations that were used in intact cells. Besides, AR had no direct effect on the activity of IKK-β that was extracted from TNF-α-stimulated HUVECs. We also found that p47 translocation, NOX4 expression, and reactive oxygen species (ROS) levels were up-regulated before IκB phosphorylation in TNF-α-induced HUVECs. Moreover, TNF-α-enhanced IKK-β activity was also inhibited by (polyethylene glycol) PEG-catalase, N-acetylcysteine (NAC), and vitamin E. In conclusion, these results suggest that AR reduces VCAM-1 and ICAM-1 expression through NADPH oxidase-dependent IKK/NF-κB pathways in TNF-α-induced HUVECs, which finally suppress monocyte-HUVECs adhesion. This compound is potentially beneficial for early-stage atherosclerosis.
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http://dx.doi.org/10.1016/j.freeradbiomed.2014.11.004DOI Listing
January 2015