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        ACOX1 destabilizes p73 to suppress intrinsic apoptosis pathway and regulates sensitivity to doxorubicin in lymphoma cells

        ( Fei-meng Zheng ),( Wang-bing Chen ),( Tao Qin ),( Li-na Lv ),( Bi Feng ),( Yan-ling Lu ),( Zuo-quan Li ),( Xiao-chao Wang ),( Li-ju Tao ),( Hong-wen Li ),( Shu-you Li ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.9

        Lymphoma is one of the most curable types of cancer. However, drug resistance is the main challenge faced in lymphoma treatment. Peroxisomal acyl-CoA oxidase 1 (ACOX1) is the rate-limiting enzyme in fatty acid β-oxidation. Deregulation of ACOX1 has been linked to peroxisomal disorders and carcinogenesis in the liver. Currently, there is no information about the function of ACOX1 in lymphoma. In this study, we found that upregulation of ACOX1 promoted proliferation in lymphoma cells, while downregulation of ACOX1 inhibited proliferation and induced apoptosis. Additionally, overexpression of ACOX1 increased resistance to doxorubicin, while suppression of ACOX1 expression markedly potentiated doxorubicin-induced apoptosis. Interestingly, downregulation of ACOX1 promoted mitochondrial location of Bad, reduced mitochondrial membrane potential and provoked apoptosis by activating caspase-9 and caspase-3 related apoptotic pathway. Overexpression of ACOX1 alleviated doxorubicin-induced activation of caspase-9 and caspase-3 and decrease of mitochondrial membrane potential. Importantly, downregulation of ACOX1 increased p73, but not p53, expression. p73 expression was critical for apoptosis induction induced by ACOX1 downregulation. Also, overexpression of ACOX1 significantly reduced stability of p73 protein thereby reducing p73 expression. Thus, our study indicated that suppression of ACOX1 could be a novel and effective approach for treatment of lymphoma. [BMB Reports 2019; 52(9): 566-571]

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        Dynamic Compression Behavior of a Mg–Gd-Based Alloy at Elevated Temperature

        Changping Tang,Kai Wu,Wenhui Liu,Di Feng,Guoliang Zuo,Wuying Liang,Yue Yang,Xu Chen,Quan Li,Xiao Liu 대한금속·재료학회 2021 METALS AND MATERIALS International Vol.27 No.6

        The dynamic compression behavior and microstructure evolution at 400 °C of an extruded Mg–8Gd–4Y–Nd–Zr alloy withdifferent tempers were investigated. The peak-aged samples exhibit the highest compressive strength, followed by as-extrudedsamples and over-aged samples. The highest dynamic compressive strength of 582 MPa was achieved by peak-aged samplecompressed at 1224 s−1. The high strength was attributed to the formation of abundant thermally stable βʹ precipitates andsome dynamic precipitates. The dynamic compressive strength of peak-aged sample and over-aged sample is not sensitiveto strain rates, while that of the as-extruded sample is sensitive to strain rates. The dynamic compressive strength of the asextrudedalloy can reach 535 MPa when compressed at 2024 s−1. The high strength was mainly ascribed to the formationof numerous dynamic precipitates and the work hardening effect caused by dislocations. The cracks are composed of crackthat is 45° to loading direction on the cylindrical surface and crack on the compressed surface. Microstructure observationindicates that the crack was easily propagated along the interface between the adiabatic shear band and matrix, grainboundaries. The equilibrium phase β in over-aged sample was unable to hinder the crack propagation.

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