Hasan Adria, Rizvi Suroor Fatima, Parveen Sana, Pathak Neelam, Nazir Aamir, Mir Snober S
Molecular Cell Biology Laboratory, Integral Information and Research Centre-4 (IIRC-4), Integral University, Lucknow, India.
Department of Bioengineering, Faculty of Engineering, Integral University, Lucknow, India.
Front Oncol. 2022 Mar 10;12:852424. doi: 10.3389/fonc.2022.852424. eCollection 2022.
Cancer formation is a highly regulated and complex process, largely dependent on its microenvironment. This complexity highlights the need for developing novel target-based therapies depending on cancer phenotype and genotype. Autophagy, a catabolic process, removes damaged and defective cellular materials through lysosomes. It is activated in response to stress conditions such as nutrient deprivation, hypoxia, and oxidative stress. Oxidative stress is induced by excess reactive oxygen species (ROS) that are multifaceted molecules that drive several pathophysiological conditions, including cancer. Moreover, autophagy also plays a dual role, initially inhibiting tumor formation but promoting tumor progression during advanced stages. Mounting evidence has suggested an intricate crosstalk between autophagy and ROS where they can either suppress cancer formation or promote disease etiology. This review highlights the regulatory roles of autophagy and ROS from tumor induction to metastasis. We also discuss the therapeutic strategies that have been devised so far to combat cancer. Based on the review, we finally present some gap areas that could be targeted and may provide a basis for cancer suppression.
癌症形成是一个高度调控且复杂的过程，很大程度上依赖于其微环境。这种复杂性凸显了根据癌症表型和基因型开发新型靶向治疗方法的必要性。自噬是一种分解代谢过程，通过溶酶体清除受损和有缺陷的细胞物质。它在诸如营养剥夺、缺氧和氧化应激等应激条件下被激活。氧化应激由过量的活性氧（ROS）诱导产生，ROS是驱动包括癌症在内的多种病理生理状况的多面分子。此外，自噬也发挥双重作用，最初抑制肿瘤形成，但在晚期促进肿瘤进展。越来越多的证据表明自噬与ROS之间存在复杂的相互作用，它们既可以抑制癌症形成，也可以促进疾病发生发展。本综述强调了自噬和ROS从肿瘤诱导到转移的调控作用。我们还讨论了迄今为止设计出的对抗癌症的治疗策略。基于该综述，我们最后提出了一些可作为靶点的空白领域，这些领域可能为癌症抑制提供基础。
