2022年4月26日 · We now report that p53R273H, but not the p53R175H hotspot mutant, interacts with SQSTM1/p62 and promotes cancer cell migration and invasion in a p62-dependent manner. Mechanistically, the p53R273H-p62 axis drives the proteasomal degradation of several cell junction–associated proteins, including the gap junction protein Connexin 43 ...

2022年2月25日 · P53 mutation status is required for the dual regulation of p62 on ferroptosis. In wild-type p53 GBM, the classical p62-mediated NRF2 activation pathway plays a major regulatory role of ferroptosis, leading to increased SLC7A11 expression, resulting in a anti-ferroptosis role.

p53因为氧化应激、dna损伤等原因而激活后就会想尽办法阻碍细胞周期继续进行，这么做的目的是给细胞提供充足的时间来修复损坏的dna。 如果修复失败——有一些这样的事件就会导致细胞出现癌变倾向——p53就会诱导细胞凋亡。

2022年3月18日 · We found that the combined use of the proteasome inhibitor epoxomicin and cisplatin led to the accumulation of p53 and sequestosome1 (p62) in the mitochondria, downregulated mitochondrial DNA (mtDNA) transcription, inhibited mitochondrial functions, and ultimately promoted apoptosis by enhancing cisplatin sensitivity in ovarian cancer cells.

We report that p53 R273H, the most common p53 mutant in pancreatic cancer, interacts with the SQSTM1/p62 protein to accelerate the degradation of cell adhesion proteins. This enables pancreatic cancer cells to detach from the epithelial sheet and engage in individualized cell migration, probably augmenting metastatic spread.

2018年1月19日 · Thus pifithrin-α-mediated blockade of p53 transcriptional activity enhances LC3 maturation and reduces p62, TIM23, TOM20 and HSP60 protein levels. This pifithrin-α-associated pro-mitophagy...

p53 immunoreactivity was present in about half the cases of non-Hodgkin's lymphoma and was related to the grade of malignancy and possibly to the B or T cell origin of the tumour. It was also associated with the proliferation state as expressed by PCNA LI and c-myc p62 expression, indicating that th …

2022年3月18日 · We found that the combined use of the proteasome inhibitor epoxomicin and cisplatin led to the accumulation of p53 and sequestosome1 (p62) in the mitochondria, downregulated mitochondrial DNA (mtDNA) transcription, inhibited mitochondrial functions, and ultimately promoted apoptosis by enhancing cisplatin sensitivity in ovarian cancer cells.

We found that the combined use of the proteasome inhibitor epoxomicin and cisplatin led to the accumulation of p53 and sequestosome1 (p62) in the mitochondria, downregulated mitochondrial DNA (mtDNA) transcription, inhibited mitochondrial functions, and ultimately promoted apoptosis by enhancing cisplatin sensitivity in ovarian cancer cells.

在这项研究中，我们根据 p53 状态揭示了 p62 在胶质母细胞瘤 (GBM) 铁死亡中的双重作用。 方法通过脂质过氧化分析、透射电子显微镜（TEM）、GSH法测定铁死亡水平。