研究动态
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APR3在癌症中的作用:细胞凋亡、自噬、氧化应激和癌症治疗。

Role of APR3 in cancer: apoptosis, autophagy, oxidative stress, and cancer therapy.

发表日期:2023 Aug 27
作者: Ping Zhang, Chaoting Zhou, Qiangan Jing, Yan Gao, Lei Yang, Yanchun Li, Jing Du, Xiangmin Tong, Ying Wang
来源: Apoptosis : an international journal on programmed cell death

摘要:

最近发现了与凋亡相关蛋白3(APR3)基因与凋亡相关的蛋白3(APR3)基因与凋亡相关的蛋白3(APR3)基因的相关性。该基因位于人类2号染色体上的2p22.3位置,包含转膜和表皮生长因子(EGF)样结构域。此外,它还具有结构位点,包括AP1、SP1和MEF2D,预示着NFAT(活化T细胞核因子)和NF-κB(κ-B核因子)可能是该基因的转录因子。功能上,APR3通过诱导线粒体损伤释放线粒体细胞色素C而参与凋亡。与此同时,APR3通过改变Cyclin D1的表达从而影响细胞周期,进而影响恶性肿瘤的发生和生长,同时促进细胞分化。早期的研究表明APR3位于溶酶体膜中,在溶酶体活性和自噬中起到作用。虽然需进一步研究以确定APR3的确切作用和分子机制,但早期的研究已经为APR3的研究奠定了基础。越来越多的证据支持APR3在肿瘤学中的重要性。因此,本综述目的在于审查对新发现的APR3在肿瘤发生中的作用的当前知识,并提供新的见解和未来研究的建议。© 2023该作者,受斯普林格科学与商业传媒有限公司的独家许可,属于斯普林格自然出版集团的一部分。
APR3 (Apoptosis-related protein 3) is a gene that has recently been identified to be associated with apoptosis. The gene is located on human chromosome 2p22.3 and contains both transmembrane and EGF (epidermal growth factor)-like domains. Additionally, it has structural sites, including AP1, SP1, and MEF2D, that indicate NFAT (nuclear factor of activated T cells) and NF-κB (nuclear factor kappa-B) may be transcription factors for this gene. Functionally, APR3 participates in apoptosis due to the induction of mitochondrial damage to release mitochondrial cytochrome C. Concurrently, APR3 affects the cell cycle by altering the expression of Cyclin D1, which, in turn, affects the incidence and growth of malignancies and promotes cell differentiation. Previous reports indicate that APR3 is located in lysosomal membranes, where it contributes to lysosomal activity and participates in autophagy. While further research is required to determine the precise role and molecular mechanisms of APR3, earlier studies have laid the groundwork for APR3 research. There is growing evidence supporting the significance of APR3 in oncology. Therefore, this review aims to examine the current state of knowledge on the role of the newly discovered APR3 in tumorigenesis and to generate fresh insights and suggestions for future research.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.