PDF(Pubmed)
Abstract：
TP53 (or p53) is widely accepted to be a tumor suppressor. Upon various cellular stresses, p53 mediates cell cycle arrest and apoptosis to maintain genomic stability. p53 is also discovered to suppress tumor growth through regulating metabolism and ferroptosis. However, p53 is always lost or mutated in human and the loss or mutation of p53 is related to a high risk of tumors. Although the link between p53 and cancer has been well established, how the different p53 status of tumor cells help themselves evade immune response remains largely elusive. Understanding the molecular mechanisms of different status of p53 and tumor immune evasion can help optimize the currently used therapies. In this context, we discussed the how the antigen presentation and tumor antigen expression mode altered and described how the tumor cells shape a suppressive tumor immune microenvironment to facilitate its proliferation and metastasis.
摘要：
TP53(或p53)被广泛认为是肿瘤抑制因子。在各种细胞压力下，p53介导细胞周期阻滞和细胞凋亡维持基因组稳定。还发现p53通过调节代谢和铁凋亡来抑制肿瘤生长。然而,p53在人类中总是丢失或突变,并且p53的丢失或突变与肿瘤的高风险有关。尽管p53和癌症之间的联系已经很好地确定，肿瘤细胞的不同p53状态如何帮助自己逃避免疫反应仍然很难理解。了解p53的不同状态和肿瘤免疫逃避的分子机制可以帮助优化当前使用的疗法。在这种情况下，我们讨论了抗原提呈和肿瘤抗原表达模式如何改变，并描述了肿瘤细胞如何塑造抑制性肿瘤免疫微环境以促进其增殖和转移。
