Bladder cancer is a disease that negatively affects patients’ quality of life, but treatment options have remained unchanged for a long time. Although promising results have been achieved with current bladder cancer treatments, cancer recurrence, progression, and therapy resistance are the most severe problems preventing the efficiency of bladder cancer treatments. Autophagy refers to an evolutionarily conserved catabolic process in which proteins, damaged organelles, and cytoplasmic components are degraded by lysosomal enzymes. Autophagy regulates the therapeutic response to the chemotherapy drugs, thus determining the effect of therapy on cancer cells. Autophagy is a stress-induced cell survival mechanism and its excessive stimulation can cause resistance of tumor cells to therapeutic agents. Depending on the conditions, an increase in autophagy may cause treatment resistance or autophagic cell death, and it is related to important anti-cancer mechanisms, such as apoptosis. Therefore, understanding the roles of autophagy under different conditions is important for designing effective anti-cancer agents. The dual role of autophagy in cancer has attracted considerable attention in respect of bladder cancer treatment. In this review, we summarize the basic characteristics of autophagy, including its mechanisms, regulation, and functions, and we present examples from current studies concerning the dual role of autophagy in bladder cancer progression and therapy.

Impact statement

Autophagy acts as an intracellular recycling system. Infection and mitochondrial damage, maintaining cellular homeostasis, orchestrating nutrient stress, hypoxia, and oxidative stress are some of the physiological roles associated with autophagy. Autophagy has also context-dependent roles in cancer. Autophagy has a significant impact on tumor initiation and promotion, with both tumor-suppressive and tumor-promoting roles. Unfortunately, conventional systemic chemotherapy for cancer therapy has been reported to have primary limitations such as chemo-resistance of targeted cells. The cytoprotective role of autophagy has been postulated as one of the causes of this resistance. Hence, combination therapy using autophagy inhibitors has recently started to emerge as a noteworthy strategy in the treatment of cancer. Therefore, targeting the autophagy pathways may be a potential therapeutic strategy for addressing cancer progression or therapy resistance in the near future. This review will provide a novel insight to understanding the paradoxical roles of autophagy in tumor suppression and tumor promotion.

中文翻译：

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自噬在膀胱癌治疗中的对比作用。

膀胱癌是一种对患者生活质量产生负面影响的疾病，但治疗方案长期以来一直保持不变。尽管目前的膀胱癌治疗已经取得了可喜的结果，但癌症复发、进展和治疗耐药性是阻碍膀胱癌治疗效率的最严重问题。自噬是一种进化上保守的分解代谢过程，其中蛋白质、受损细胞器和细胞质成分被溶酶体酶降解。自噬调节对化疗药物的治疗反应，从而决定治疗对癌细胞的影响。自噬是一种应激诱导的细胞存活机制，其过度刺激会导致肿瘤细胞对治疗药物产生耐药性。根据条件，自噬的增加可能导致治疗抵抗或自噬细胞死亡，这与细胞凋亡等重要的抗癌机制有关。因此，了解自噬在不同条件下的作用对于设计有效的抗癌药物非常重要。自噬在癌症中的双重作用在膀胱癌治疗方面引起了相当大的关注。在这篇综述中，我们总结了自噬的基本特征，包括其机制、调控和功能，并提供了当前研究中关于自噬在膀胱癌进展和治疗中的双重作用的例子。了解自噬在不同条件下的作用对于设计有效的抗癌药物很重要。自噬在癌症中的双重作用在膀胱癌治疗方面引起了相当大的关注。在这篇综述中，我们总结了自噬的基本特征，包括其机制、调控和功能，并提供了当前研究中关于自噬在膀胱癌进展和治疗中的双重作用的例子。了解自噬在不同条件下的作用对于设计有效的抗癌药物很重要。自噬在癌症中的双重作用在膀胱癌治疗方面引起了相当大的关注。在这篇综述中，我们总结了自噬的基本特征，包括其机制、调控和功能，并提供了当前研究中关于自噬在膀胱癌进展和治疗中的双重作用的例子。

影响陈述

自噬充当细胞内循环系统。感染和线粒体损伤、维持细胞稳态、协调营养应激、缺氧和氧化应激是与自噬相关的一些生理作用。自噬在癌症中也具有上下文相关的作用。自噬对肿瘤的发生和促进具有显着影响，具有抑制肿瘤和促进肿瘤的作用。不幸的是，据报道，用于癌症治疗的常规全身化疗具有主要局限性，例如靶向细胞的化学抗性。自噬的细胞保护作用被认为是这种抗性的原因之一。因此，使用自噬抑制剂的联合疗法最近开始成为治疗癌症的一个值得注意的策略。所以，靶向自噬途径可能是在不久的将来解决癌症进展或治疗耐药性的潜在治疗策略。本综述将为理解自噬在肿瘤抑制和肿瘤促进中的矛盾作用提供新的见解。