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Regulation of p53 stability as a therapeutic strategy for cancer

机译：调节P53作为癌症治疗策略的稳定性

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The tumor suppressor protein p53 participates in the control of key biological functions such as cell death, metabolic homeostasis and immune function, which are closely related to various diseases such as tumors, metabolic disorders, infection and neurodegeneration. The p53 gene is also mutated in approximately 50% of human cancer cells. Mutant p53 proteins escape from the ubiquitination-dependent degradation, gain oncogenic function and promote the carcinogenesis, malignant progression, metastasis and chemoresistance. Therefore, the stability of both wild type and mutant p53 needs to be precisely regulated to maintain normal functions and targeting the p53 stability is one of the therapeutic strategies against cancer. Here, we focus on compoundinduced degradation of p53 by both the ubiquitination-dependent proteasome and autophagy-lysosome degradation pathways. We also review other posttranslational modifications which control the stability of p53 and the biological functions involved in these processes. This review provides the current theoretical basis for the regulation of p53 abundance and its possible applications in different diseases.
机译：肿瘤抑制蛋白P53参与控制关键生物学功能，例如细胞死亡，代谢稳态和免疫功能，这与肿瘤，代谢紊乱，感染和神经变性等各种疾病密切相关。 P53基因也突变为约50％的人癌细胞。突变体P53蛋白逃离泛素化依赖性降解，增益致癌功能并促进致癌，恶性进展，转移和化学性。因此，需要精确调节野生型和突变体P53的稳定性以维持正常功能并靶向P53稳定性是对癌症的治疗策略之一。在这里，我们专注于泛素依赖性蛋白酶体和自噬 - 溶酶体降解途径的P53的复合降解。我们还审查了其他后期修改，可控制P53的稳定性和这些过程所涉及的生物学功能。本综述提供了当前对P53丰度的定期理论依据及其在不同疾病中可能的应用。

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