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Ferroptosis is an iron-dependent oxidative, nonapoptotic form of regulated cell death caused by the destruction of redox homeostasis. Recent studies have uncovered complex cellular networks that regulate ferroptosis. GINS4 is a promoter of eukaryotic G 1 /S - cell cycle as a regulator of initiation and elongation of DNA replication, but little is known about its impact on ferroptosis. Here, we found that GINS4 was involved in the regulation of ferroptosis in lung adenocarcinoma (LUAD). CRISPR/Cas9-mediated GINS4 KO facilitated ferroptosis. Interestingly, depletion of GINS4 could effectively induce G1, G 1 /S, S, and G 2 /M cells to ferroptosis, especially for G2/M cells. Mechanistically, GINS4 suppressed p53 stability through activating Snail that antagonized the acetylation of p53, and p53 lysine residue 351 (K351 for human p53) was the key site for GINS4-suppressed p53-mediated ferroptosis. Together, our data demonstrate that GINS4 is a potential oncogene in LUAD that functions to destabilize p53 and then inhibits ferroptosis, providing a potential therapeutic target for LUAD.

Background & aim Gastric cancer (GC) is the third-leading cause of cancer-related deaths. We established a prospective database of patients with GC who underwent surgical treatment. In this study, we explored the prognostic significance of the expression of CFP1 and 14-3-3 in gastric cancer, by studying the specimens collected from clinical subjects. Materials & methods Immunohistochemistry was used to detect the expression of CFP1 and 14-3-3 in 84 GC subjects, including 73 patients who have undergone radical gastrectomy and 11 patients who have not undergone radical surgery. Survival analysis was performed by km-plot data. Results According to the survival analysis, we can see that the survival time of patients with high expression of CFP1 is lower than the patients with low expression in gastric cancer, while the effect of 14-3-3 is just the opposite. The survival time of patients with higher expression of 14-3-3 is also longer. Conclusion The CFP1 and 14-3-3 genes can be used as prognostic markers in patients with GC, but the study is still needed to confirm.