Independent Researcher, India.
Department of Biochemistry, All India Institute of Medical Sciences, Bhopal, Madhya pradesh-462020, India.
Anticancer Agents Med Chem. 2021 Oct 28;21(16):2130-2141. doi: 10.2174/1871520621666210112121910.
The term Mitophagy has been newly concerned in reforming the metabolic landscape inside cancerous cells in addition to the interface between malignant cells as well as other major constituents of tumour microenvironment. Several profoundly interrelated systems, comprising mitochondrial dynamics and mitophagy, function in mammalian cells as vital mitochondrial regulator processes, and their consequence in neoplastic development has recently been illuminated clinically. In specific instances of cancer cells, mitochondrial-protected metabolic paths are revamped to meet expanded bioenergetics along with biosynthetic necessities of malignant cells, in addition to deal with oxidative stress. It is an exhausting task to foresee the role that mitophagy has on malignant growth cells since it relies upon various elements like cancer variability, malignant growth phase, genetic background and harmony between cell demand and accessibility. As per condition, mitophagy may have a double role as cancer suppressor for example Atg5 (autophagy related 5) or Atg7 (autophagy related 7) or execute promoter like function for instance FUNDC1 (FUN14 domain-containing protein 1), BNIP3 (BCL2/adenovirus E1B 19-kDa-interacting protein 3), PINK1 (PTEN-instigated kinase 1) etc. Tumour suppressive function of Parkin (E3 ubiquitin ligase) is likewise distinguished in mammary gland carcinoma where obstruction of mitophagy impacts tumour progression. In pancreatic cancer cells and hepatocellular carcinoma hypermethylation of the BNIP3, promoter occurs that prevent HIF-1 (Hypoxia-Inducible Factor 1) binding besides ensuing initiation of mitophagy. Since the dual role of mitophagy has in malignant growth relying upon various circumstances and cell varieties, a range of studies have been performed on mitophagy and its role in cancer progression and development is opening up a new paradigm with immense clinical importance.
自噬一词最近受到关注，它不仅可以重塑癌变细胞内的代谢状态，还可以调节癌细胞与肿瘤微环境中其他主要成分之间的相互作用。在哺乳动物细胞中，几个相互关联的系统，包括线粒体动力学和自噬，作为重要的线粒体调节过程发挥作用，其在肿瘤发生中的作用最近已在临床上得到阐明。在某些癌细胞中，为了满足恶性细胞不断扩展的生物能量和生物合成需求，以及应对氧化应激，线粒体保护的代谢途径会被重新构建。自噬对恶性生长细胞的作用难以预测，因为它依赖于多种因素，如癌症的异质性、肿瘤的阶段、遗传背景以及细胞需求和可及性之间的平衡。根据具体情况，自噬可能具有双重作用，例如作为抑癌基因（如 Atg5 或 Atg7），或者执行促进作用，例如 FUNDC1、BNIP3、PINK1 等。Parkin（E3 泛素连接酶）在乳腺癌中的抑癌功能也有区别，其中自噬的阻断会影响肿瘤的进展。在胰腺癌细胞和肝细胞癌中，BNIP3 的启动子发生 hypermethylation，阻止 HIF-1（缺氧诱导因子 1）结合，从而引发自噬的起始。由于自噬在肿瘤生长中的双重作用取决于各种情况和细胞类型，因此已经进行了多项关于自噬及其在癌症进展和发展中的作用的研究，这为癌症研究开辟了一个具有巨大临床重要性的新范例。
