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首页> 外文期刊>Expert opinion on therapeutic targets >Sequestosome 1/p62-related pathways as therapeutic targets in hepatocellular carcinoma
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Sequestosome 1/p62-related pathways as therapeutic targets in hepatocellular carcinoma

机译：与肝细胞癌的治疗靶标有关的杀囊肿1 / p62相关途径

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Introduction: Protein sequestosome 1/p62 (p62) plays a crucial role in vital complex and interacting signaling pathways in normal and neoplastic cells. P62 is involved in autophagy, defense against oxidative stress via activation of the Keap1/Nrf2 system, in protein aggregation and sequestration, and in apoptosis. Autophagy contributes to cell survival and proliferation by eliminating damaged organelles, potentially toxic protein aggregates and invading microorganisms, and by providing nutrients under starvation conditions. The same holds true for oxidative stress defense, which may prevent genomic alterations and tumor initiation but also protect established tumor cells and promote tumor progression. Cross-talk between autophagy and apoptosis is regulated by a signaling network with the involvement of p62. Areas covered: The review deals with structure, function, and regulation of p62 and its role in liver carcinogenesis. Emphasis is placed on mechanisms leading to overexpression of p62 and its accumulation as inclusion bodies in HCC and on the impact of p62-dependent signaling pathways in tumor cells with the aim to explore the possible role of p62 as the therapeutic target. Expert opinion: Depending on the context, targeting p62 or interference with related pathways, such as autophagy, is a potential therapeutic strategy in HCC. However, the heterogeneity of this tumor entity and the complexity and mutual interactions of the p62-dependent pathways involved are challenges for a targeted therapy since interference with p62-mediated regulatory processes could result likewise in inhibition of tumorigenesis and in its promotion and thus provoke harmful side effects. Therapy-related patient stratification based on reliable markers to better define pathogenic principles of the tumor is a necessity when this type of treatment is considered.
机译：介绍：蛋白杀蛋白酶体1 / p62（p62）在生命复合物中起着至关重要的作用，在正常和肿瘤细胞中相互作用。 P62涉及自噬，通过激活Keap1 / NRF2系统，在蛋白质聚集和封存中和凋亡中进行氧化应激。自噬通过消除受损的细胞器，潜在有毒蛋白质聚集体和入侵微生物有助于细胞存活和增殖，并通过在饥饿条件下提供营养物质。对于氧化胁迫防御，这也是如此，这可能会阻止基因组改变和肿瘤起始，但也保护已建立的肿瘤细胞并促进肿瘤进展。自噬和细胞凋亡之间的串扰是由信号网络调节，其中P62的参与。所涵盖的区域：审查涉及P62的结构，功能和调节及其在肝癌中的作用。重点置于导致P62过表达的机制及其作为HCC的包涵体的积累以及P62依赖性信号通路在肿瘤细胞中的影响，目的是探讨P62作为治疗靶标的可能作用。专家意见：根据上下文，针对相关途径的靶向P62或诸如自噬的干扰，是HCC潜在的治疗策略。然而，这种肿瘤实体的异质性和所涉及的P62依赖性途径的复杂性和相互相互作用是针对性治疗的挑战，因为与p62介导的调节过程的干扰同样可以抑制肿瘤发生和促销，因此引发有害副作用。基于可靠标记的治疗相关患者分层以更好地定义肿瘤的致病原理是必要的，这是考虑这种类型的处理。

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