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TRAF7 enhances degradation of ubiquitinated KLF4 to promote hepatocellular carcinoma progression

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Cancer Biology & Medicine 2018年第S1期15卷 8-8页

作者： Huan He Zhiyuan Wu Sheng Li Dongmei Wang Zhihua Liu Chunfeng Qu Cancer Hospital Chinese Academy of Medical SciencesBeijingChina

Objective:The tumor necrosis factor receptor-associated factor 7(TRAF7)is one of the components of the tumor necrosis factor alpha(TNF-α)/nuclear factor kappa B(NF-κB)pathway and a putative E3-ubiquitin *** study aims to explore the biologic effects and the molecular mechanisms of deregulated TRAF7 signaling in hepatocellular carcinoma(HCC)progression.

关键词： TRAF7 enhances degradation

3-70 Capsazepine, a TRPV1 Antagonist, enhances Radiation Sensitivity in Human Hepatocellular Carcinoma HepG2 Cells

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IMP & HIRFL Annual Report 2014年第1期 162-163页

作者： Han Lu Di Cuixia Zhang Hong 不详

Transient receptor potential vanilloid 1(TRPVl) that is known as capsaicin receptor is a non-selective cationion channel[1]. TRPV1 can regulate Ca2+ influx, participate in a variety of physiological and pathological processof tumor[2]. One such agent is Capsazepine (CPZ) that is now widely used as a selective vanilloid type 1 receptor(TRPV1) antagonist. CPZ can be directly actived on the capsaicin receptor, blocked its biological effects, and abolishedosteosarcoma-induced hyperalgesia when administered subcutaneously at doses ranging from 3 to 10 mg/kg,blocked calcium channels[3]. However, the mechanisms underlying the anticancer effects of CPZ have not fully beenunderstood. Whether CPZ can induce apoptosis of human hepatocellular carcinoma cell line HepG2 is not ***, the objective of the study reported here was to determine whether CPZ can enhance radiation sensitivityin HepG2 cell, and impact on cell proliferation.

关键词： TRPV1 enhances Radiation

3-69 MiR-449a enhances Radiosensitivity by Downregulation of c-Myc in Prostate Cancer Cells

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IMP & HIRFL Annual Report 2015年第1期 172-174页

作者： Mao Aihong Zhang Hong Zhou Rong 不详

c-Myc was one of the first oncogenes to be identified and its overexpression at the RNA and protein levels has subsequently been linked to a wide variety of human cancers[1]. Overexpression of the c-Myc protein or c-Myc gene has been shown in 80% of breast cancers, 70% of colon cancers, 90% of gynecological cancers, 50% of hepatocellular carcinomas and a variety of hematological tumors.

关键词： MiR-449a enhances Radiosensitivity

3-68 Loss of Nrf2 enhances the Radiosensitivity in Human Lung Cancer Cells

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IMP & HIRFL Annual Report 2014年第1期 161-161页

作者： Zhao Qiuyue Zhang Hong 不详

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial transcription factor regulating the expression ofantioxidant genes. Under oxidative stress conditions or other stimulus, Nrf2 translocating from the cytoplasminto the nucleus, binds to antioxidant response elements, and increases the expression of antioxidant enzymes[1;2].Constitutive Nrf2 activation in many tumors enhances cell survival and resistance. For instance, high level of Nrf2 isobserved in non-small cell lung cancer A549 cells[3;4]. The gain of Nrf2 function has been implicated in the resistanceof cancer cells to radiation therapy.

关键词： Nrf2 enhances Radiosensitivity

3-67 MiR-449a Overexpression enhances the Radiosensitivity in Prostate Cancer Cells

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IMP & HIRFL Annual Report 2014年第1期 160-161页

作者： Mao Aihong Liu Yang Zhang Hong 不详

Multiple links between miRNA activity and cancer have been established. Several miRNAs have been describedas oncogenes while others act as tumour suppressors[1]. MiR-449a is a member of miR-34 family which locates onhuman chromosome 5q11.2, a region identified as a susceptibility locus in a variety of malignancies, includingprostate cancer[2]. In line with the tumor-suppressive role of miR-34, miR-449a was shown to be significantly downregulatedin prostate cancer cell lines and tissue relative to normal tissues and plays a critical role in growth ofprostate cancer cells [3;4].

关键词： Overexpression enhances Radiosensitivity

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壁报及其它摘要

神经药理学报 2019年第2期9卷 118-130页

OA-1 CXCR2 Antagonism Promotes Oligodendrocyte Precursor Cell Differentiation and enhances Remyelination in A Mouse Model of Multiple Sclerosis WANG Lu,YANG Han-yu,ZANG Cai-xia,DONG Yi,SHANG Jun-mei,CHEN Jia-jing,WANG Yue,LIU Hui, ZHANG Zi-hong,XU Heng,BAO Xiu-qi,ZHANG Dan State Key Laboratory of Natural Products and Functions,Institute of Materia Medica,Chinese Academy of Medical Sciences & Peking Union Medical College,Beijing,100050,China 【ABSTRACT】 Multiple sclerosis(MS) is a chronic autoimmune demyelinating disease characterized by the autoimmune attack of oligodendrocytes,leading to demyelination and progressive functional deficits. CXC chemokine receptor 2 (CXCR2) is recently reported to orchestrate the migration,proliferation and differentiation of oligodendrocyte precursor cells (OPCs),which implies its possible involvement in the demyelinating process. Here,we used a CXCR2 antagonist,compound 2,as a tool to investigate the role of CXCR2 in demyelination and the underlying mechanism. The primary cultured oligodendrocytes and cuprizone (CPZ)- intoxicated mice were applied in the present study.

关键词： Oligodendrocyte Precursor Cell enhances Remyelination