Ferroptosis is a form of iron-dependent programmed cell death (PCD) that, once activated, inhibits tumor progression. However, the specific mechanisms influencing ferroptosis in nasopharyngeal carcinoma (NPC) are limited and warrant further investigation. This study proposes that MICAL2 not only influences the nuclear translocation of p53 but also facilitates the ubiquitination of p53 by recruiting the E3 ubiquitination ligase MDM2, leading to its degradation. This process inhibits ferroptosis in NPC cells, thereby promoting NPC progression and adversely affecting the prognosis of NPC patients. Additionally, we identified a novel long non-coding RNA (lncRNA), LINC-AC092535.5, which directly modulates the MICAL2 mRNA level through dual reinforcement at both transcriptional and post-transcriptional levels. Transcriptome sequencing and RACE experiments provided insights into the function of this new lncRNA. These findings will contribute to the expansion of the ferroptosis gene regulatory network and inform new clinical treatment strategies for NPC.
Zhang et al. (Sat,) studied this question.