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Search Results (28)
  • Open Access


    TIPE2 Inhibits Hypoxia-Induced Wnt/β-Catenin Pathway Activation and EMT in Glioma Cells

    Zhi-jun Liu*1, Hong-lin Liu*1, Hai-cun Zhou, Gui-cong Wang*

    Oncology Research, Vol.24, No.4, pp. 255-261, 2016, DOI:10.3727/096504016X14666990347356

    Abstract Hypoxia-induced epithelial-to-mesenchymal transition (EMT) could facilitate tumor progression. TIPE2, the tumor necrosis factor-α (TNF-α)-induced protein 8-like 2 (also known as TNFAIP8L2), is a member of the TNF-α-induced protein 8 (TNFAIP8, TIPE) family and has been involved in the development and progression of several tumors. However, the effects of TIPE2 on the EMT process in glioma cells and the underlying mechanisms of these effects have not been previously reported. In our study, we assessed the roles of TIPE2 in the EMT process in glioma cells in response to hypoxia. Our results indicated that TIPE2 expression was More >

  • Open Access


    MicroRNA-33b Inhibits the Proliferation and Migration of Osteosarcoma Cells via Targeting Hypoxia-Inducible Factor-1α

    Yong Zhou, Chuandong Yang, Kunpeng Wang, Xuefeng Liu, Quan Liu

    Oncology Research, Vol.25, No.3, pp. 397-405, 2017, DOI:10.3727/096504016X14743337535446

    Abstract Recently, microRNA (miR)-33b has been demonstrated to act as a tumor suppressor in osteosarcoma. However, the regulatory mechanism of miR-33b in osteosarcoma cell proliferation and migration remains largely unknown. In this study, real-time PCR showed that miR-33b was significantly downregulated in osteosarcoma tissues compared to their matched adjacent nontumor tissues. Its expression was also decreased in several common osteosarcoma cell lines, including Saos-2, MG63, U2OS, and SW1353, when compared to normal osteoblast cell line hFOB. Overexpression of miR-33b suppressed U2OS cell proliferation and migration. HIF-1α was further identified as a target of miR-33b, and its… More >

  • Open Access


    Overexpression of miR-140 Inhibits Proliferation of Osteosarcoma Cells via Suppression of Histone Deacetylase 4

    Qianren Xiao*1, Lu Huang†1, Zhongzu Zhang‡1, Xiang Chen*, Jiaquan Luo*, Zhanmin Zhang§, Shaoqing Chen§, Yong Shu*, Zhimin Han*, Kai Cao*

    Oncology Research, Vol.25, No.2, pp. 267-275, 2017, DOI:10.3727/096504016X14732510786564

    Abstract miRNAs play a pivotal role in the development and progression of osteosarcoma (OS). Previous studies indicated that miR-140 acts as a tumor suppressor in many cancers. However, its accurate expression and exact function in OS cells remain unknown. Herein, we demonstrated the lower expression of miR-140 in 40 paired OS tissues. Restoring miR-140 expression in OS cells had a marked effect on inhibiting cell proliferation and invasion, inducing cell apoptosis in vitro, and suppressing tumor growth in vivo. Moreover, a bioinformatics prediction indicated that the histone deacetylase 4 (HDAC4) is a target gene of miR-140 and More >

  • Open Access


    Phosphoglycerate Mutase 1 (PGAM1) Promotes Pancreatic Ductal Adenocarcinoma (PDAC) Metastasis by Acting as a Novel Downstream Target of the PI3K/Akt/mTOR Pathway

    Xinlu Liu, Xiaodong Tan, Peng Liu, Yunhao Wu, Songying Qian, Xiaobo Zhang

    Oncology Research, Vol.26, No.7, pp. 1123-1131, 2018, DOI:10.3727/096504018X15166223632406

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive tumors known, with an overall 5-year survival rate of less than 6% due to early local invasion and distant metastasis. Exploring suitable therapeutic targets associated with invasion and metastasis is required for improving the prognosis of PDAC. In this study, we investigated the role of the glycolytic enzyme phosphoglycerate mutase 1 (PGAM1) in PDAC. PGAM1 expression was examined in tissue samples of 54 PDAC patients using immunohistochemistry, and the correlation between clinicopathological expression and PGAM1 expression was determined. A survival curve was generated using the… More >

  • Open Access


    MicroRNA-519d-3p Inhibits Proliferation and Promotes Apoptosis by Targeting HIF-2α in Cervical Cancer Under Hypoxic Conditions

    Lixia Jiang*1, Shaohua Shi†1, Qiaofa Shi, Huijuan Zhang*, Yu Xia§, Tianyu Zhong*

    Oncology Research, Vol.26, No.7, pp. 1055-1062, 2018, DOI:10.3727/096504018X15152056890500

    Abstract HIF-2α knockdown inhibits proliferation, arrests the cell cycle, and promotes apoptosis and autophagy under hypoxic conditions in cervical cancer. However, the upstream regulatory mechanism of HIF-2α expression is unclear. MicroRNAs (miRNAs) degrade target mRNAs by binding to the 3'-untranslated region of mRNAs. In this study, we investigated the role of miRNAs in the regulation of HIF-2α expression in cervical cancer under hypoxic conditions. miRNAs regulating HIF-2α expression were predicted using TargetScan and miRanda and were determined in cervical cancer under hypoxic conditions by qRT-PCR. Additionally, the targeted regulation of HIF-2α by miR-519d-3p was evaluated by… More >

  • Open Access


    Detection of Necroptosis in Ligand-Mediated and Hypoxia-Induced Injury of Hepatocytes Using a Novel Optic Probe-Detecting Receptor-Interacting Protein (RIP)1/RIP3 Binding

    Sanae Haga*, Akira Kanno, Takeaki Ozawa, Naoki Morita§, Mami Asano,¶ and Michitaka Ozaki

    Oncology Research, Vol.26, No.3, pp. 503-513, 2018, DOI:10.3727/096504017X15005102445191

    Abstract Liver injury is often observed in various pathological conditions including posthepatectomy state and cancer chemotherapy. It occurs mainly as a consequence of the combined necrotic and apoptotic types of cell death. In order to study liver/hepatocyte injury by the necrotic type of cell death, we studied signal-regulated necrosis (necroptosis) by developing a new optic probe for detecting receptor-interacting protein kinase 1 (RIP)/RIP3 binding, an essential process for necroptosis induction. In the mouse hepatocyte cell line, TIB-73 cells, TNF-a/cycloheximide (T/C) induced RIP1/3 binding only when caspase activity was suppressed by the caspase-specific inhibitor z-VAD-fmk (zVAD). T/C/zVAD-induced… More >

  • Open Access


    Stubborn Hypoxia in Neonates with D-Transposition of the Great Arteries after Arterial Switch Operation: Central Sleep Apnea as the Cause and Potential Indicator of Brain Immaturity

    Camden L. Hebson1,*, Kyle Bliton2, Amr Y. Hammouda1, Kaitlyn Barr3, W. Hampton Gray4, Mohini Gunnett2, Waldemar F. Carlo1

    Congenital Heart Disease, Vol.19, No.2, pp. 185-195, 2024, DOI:10.32604/chd.2024.048871

    Abstract D-transposition of the great arteries (d-TGA) is surgically repaired with the arterial switch operation (ASO) with excellent results, however short and long-term morbidities still develop including neurocognitive delay. Clinically significant central sleep apnea is uncommon in non-premature infants, but when present indicates immature autonomic control of respiration likely due to a neurologic disorder. We report the unanticipated finding of central sleep apnea in four-term neonates with d-TGA after uncomplicated ASO, with the short-term complication of delayed hospital discharge and long-term concerns regarding this early marker of brain immaturity and its hindrance to normal development. Within More >

  • Open Access


    HIFs in hypoxic regulation of the extracellular matrix: focus on little-known player HIF-3


    BIOCELL, Vol.48, No.5, pp. 677-692, 2024, DOI:10.32604/biocell.2024.048873

    Abstract The structural and associated molecules of the extracellular matrix (ECM) complex is an important component of the local milieu of cells, both for maintaining their functions and homeostasis. It is a dynamic structure that is finely tuned to changes in the microenvironment. One of these factors is hypoxia, which can arise in tissues due to physiological or pathological effects. As a result of the hypoxic effect, the properties of the ECM are significantly modified, stiffness increases, the balance between degradation and synthesis of structural proteins shifts, and the deposition of biologically active mediators’ changes. Hypoxia-inducible… More >

  • Open Access


    Inhibition of VEGF-A expression in hypoxia-exposed fetal retinal microvascular endothelial cells by exosomes derived from human umbilical cord mesenchymal stem cells


    BIOCELL, Vol.47, No.11, pp. 2485-2494, 2023, DOI:10.32604/biocell.2023.044177

    Abstract Objective: This study aimed to investigate the potential of human umbilical cord mesenchymal stem cell (hucMSC)-derived exosomes (hucMSC-Exos) in inhibiting hypoxia-induced cell hyper proliferation and overexpression of vascular endothelial growth factor A (VEGF-A) in immature human fetal retinal microvascular endothelial cells (hfRMECs). Methods: Exosomes were isolated from hucMSCs using cryogenic ultracentrifugation and characterized through various techniques, including transmission electron microscopy, nanoparticle tracking analysis, bicinchoninic acid assays, and western blotting. The hfRMECs were identified using von Willebrand factor (vWF) co-staining and divided into four groups: a control group cultured under normoxic condition, a hypoxic model group, a hypoxic… More > Graphic Abstract

    Inhibition of VEGF-A expression in hypoxia-exposed fetal retinal microvascular endothelial cells by exosomes derived from human umbilical cord mesenchymal stem cells

  • Open Access


    NR4A1 enhances glycolysis in hypoxia-exposed pulmonary artery smooth muscle cells by upregulating HIF-1α expression


    BIOCELL, Vol.47, No.11, pp. 2423-2433, 2023, DOI:10.32604/biocell.2023.044459

    Abstract Background: Pulmonary arterial hypertension (PAH) is a chronic and progressive disease that is strongly associated with dysregulation of glucose metabolism. Alterations in nuclear receptor subfamily 4 group A member 1 (NR4A1) activity alter the outcome of PAH. This study aimed to investigate the effects of NR4A1 on glycolysis in PAH and its underlying mechanisms. Methods: This study included twenty healthy volunteers and twenty-three PAH patients, and plasma samples were collected from the participants. To mimic the conditions of PAH in vitro, a hypoxia-induced model of pulmonary artery smooth muscle cell (PASMC) model was established. The proliferation… More > Graphic Abstract

    NR4A1 enhances glycolysis in hypoxia-exposed pulmonary artery smooth muscle cells by upregulating HIF-1α expression

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