The paradox of autophagy in cancer: NEAT1's role in tumorigenesis and therapeutic resistance

IF 2.9 4区 医学 Q2 PATHOLOGY Pathology, research and practice Pub Date : 2024-08-13 DOI:10.1016/j.prp.2024.155523
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Abstract

Cancer remains a current active problem of modern medicine, a process during which cell growth and proliferation become uncontrolled. However, the role of autophagy in the oncological processes is counterintuitive and, at the same time, increasingly influential on the formation, development, and response to therapy of oncological diseases. Autophagy is a vital cellular process that removes defective proteins and organelles and supports cellular homeostasis. Autophagy can enhance the ability to form new tumors and suppress this formation in cancer. The dual potential of apoptosis may be the reason for this duality in either promoting or impeding the survival of cancer cells, depending on the situation, including starvation or treatment stress. Furthermore, long non-coding RNA NEAT1, which has been linked to several stages of carcinogenesis and in all forms of the illness, has drawn attention as a major player in cancer biology. NEAT1 is a structural portion of nuclear paraspeckles and has roles in deactivating expression in both transcriptional and post-transcriptional levels. NEAT1 acts in carcinogenesis in numerous ways, comprising interactions with microRNAs, the influence of gene articulation, regulation of epigenetics, and engagement in signalling cascades. In addition, the complexity of NEAT1’s role in cancer occurrence is amplified by its place in regulating cancer stem cells and the tumor microenvironment. NEAT1’s interaction with autophagy further complicates the already complicated function of this RNA in cancer biology. NEAT1 has been linked to autophagy in several types of cancer, influencing autophagy pathways and altering its stress response and tumor cell viability. Understanding the interrelation between NEAT1, autophagy, and cancer will enable practitioners to identify novel treatment targets and approaches to disrupt oncogenic processes, reduce the occurrence of treatment resistance, and increase patient survival rates. Specialized treatment strategies and regimens are thus achievable. In the present review, the authors analyze sophisticated relationship schemes in cancer: The NEAT1 pathway and the process of autophagy.

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癌症中的自噬悖论:NEAT1 在肿瘤发生和抗药性中的作用
癌症仍然是现代医学的一个活跃问题,是细胞生长和增殖失控的过程。然而,自噬在肿瘤过程中的作用却与直觉相反,同时对肿瘤疾病的形成、发展和治疗反应的影响也越来越大。自噬是一种重要的细胞过程,可清除有缺陷的蛋白质和细胞器,并支持细胞的平衡。自噬可增强形成新肿瘤的能力,也可抑制癌症的形成。细胞凋亡的双重潜能可能是造成这种双重性的原因,它可以促进或阻碍癌细胞的存活,具体取决于饥饿或治疗压力等情况。此外,长非编码 RNA NEAT1 与癌症发生的多个阶段和各种形式的疾病都有关联,它作为癌症生物学中的一个重要角色引起了人们的关注。NEAT1 是核副斑块的结构部分,在转录和转录后水平上都有去激活表达的作用。NEAT1 在致癌过程中以多种方式发挥作用,包括与 microRNA 的相互作用、基因衔接的影响、表观遗传学的调控以及信号级联的参与。此外,由于 NEAT1 在调节癌症干细胞和肿瘤微环境中的作用,其在癌症发生过程中的作用更加复杂。NEAT1 与自噬的相互作用使这种 RNA 在癌症生物学中本已复杂的功能变得更加复杂。在几种癌症中,NEAT1 都与自噬有关,它影响自噬途径,改变应激反应和肿瘤细胞的活力。了解 NEAT1、自噬和癌症之间的相互关系将有助于医生确定新的治疗靶点和方法,以破坏致癌过程、减少耐药性的发生并提高患者的存活率。因此,专门的治疗策略和方案是可以实现的。在本综述中,作者分析了癌症中的复杂关系方案:NEAT1途径和自噬过程。
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来源期刊
CiteScore
5.00
自引率
3.60%
发文量
405
审稿时长
24 days
期刊介绍: Pathology, Research and Practice provides accessible coverage of the most recent developments across the entire field of pathology: Reviews focus on recent progress in pathology, while Comments look at interesting current problems and at hypotheses for future developments in pathology. Original Papers present novel findings on all aspects of general, anatomic and molecular pathology. Rapid Communications inform readers on preliminary findings that may be relevant for further studies and need to be communicated quickly. Teaching Cases look at new aspects or special diagnostic problems of diseases and at case reports relevant for the pathologist''s practice.
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