Reprogramming of lipid metabolism, which modulates energy utilization and cell signaling, maintains cell survival and promotes cancer metastasis in cancer cells. Ferroptosis is a type of cell necrosis caused by an overload of lipid oxidation, which has been demonstrated to be involved in cancer cell metastasis. However, the mechanism by which fatty acid metabolism regulates the anti-ferroptosis signaling pathways is not fully understood. The formation of ovarian cancer spheroids helps to counteract the hostile microenvironment of the peritoneal cavity with low oxygen, shortage of nutrients, and subjected to platinum therapy. Previously, we demonstrated that Acyl-CoA synthetase long-chain family member 1 (ACSL1) promotes cell survival and peritoneal metastases in ovarian cancer, but the mechanism is still not well elucidated. In this study, we demonstrate that the formation of spheroids and under exposure to platinum chemotherapy increased the levels of anti-ferroptosis proteins as well as ACSL1. Inhibition of ferroptosis can enhance spheroid formation and vice versa. Genetic manipulation of ACSL1 expression showed that ACSL1 reduced the level of lipid oxidation and increased the resistance to cell ferroptosis. Mechanistically, ACSL1 increased the N-myristoylation of ferroptosis suppressor 1 (FSP1), resulting in the inhibition of its degradation and translocation to the cell membrane. The increase in myristoylated FSP1 functionally counteracted oxidative stress-induced cell ferroptosis. Clinical data also suggested that ACSL1 protein was positively correlated with FSP1 and negatively correlated with the ferroptosis markers 4-HNE and PTGS2. In conclusion, this study demonstrated that ACSL1 enhances antioxidant capacity and increases ferroptosis resistance by modulating the myristoylation of FSP1.

Galangin suppresses proliferation and induces apoptosis and autophagy in hepatocellular carcinoma (HCC) cells, but the precise mechanism is not clear. In this study, we demonstrated that galangin induced autophagy, enhanced the binding of SIRT1-LC3 and reduced the acetylation of endogenous LC3 in HepG2 cells. But this autophagy was inhibited by inactivation of SIRT1 meanwhile, galangin failed to reduce the acetylation of endogenous LC3 after SIRT1 was knocked-down. Collectively, these findings demonstrate a new mechanism by which galangin induces autophagy via the deacetylation of endogenous LC3 by SIRT1.

Antimicrobial peptides (AMPs) come from various sources and exhibit unique antimicrobial properties. Their rapid action, effectiveness, and resistance to resistance development make them promising alternatives to combat antibiotic resistance. In addition to its excellent antibacterial properties, AMPs have superior immunomodulatory, antitumor, and antiviral activities. In recent years, the demand for AMPs has continued to increase in many fields, especially in the medical field, and the prospects are extensive. However, AMPs have the disadvantages of expensive development cost, higher hemolysis, short half-life, susceptibility to degradation by protein hydrolases, low bioavailability, toxic side effects, and other disadvantages, which seriously limit the wide application of AMPs. Therefore, fewer AMPs have been approved for marketing or are undergoing clinical trials. The review covers the period from 2001 to 2025 and provides a detailed discussion by searching databases such as Google Scholar and Web of Science. This paper reviews the progress of research on AMPs sources, structures, optimization strategies, biological activities, mechanisms of action, and applications. In general, the development approaches and the number of new AMPs have increased significantly. The improvement technologies for AMPs high hemolysis, poor stability, low bioavailability and high cost have increased significantly. The development cost of AMPs is still high, but many AMPs have been widely used in clinical, food, livestock, poultry, cosmetics and other fields. This article focuses on the commonly used optimization strategies and main activities of AMPs, aiming to effectively respond to challenges and provide a theoretical basis for expanding their application range.

Corroles have been previously demonstrated to be a new and promising photosensitizer (PS) in photodynamic therapy (PDT) for cancer cells. This research reported the preparation of an electron-deficient flat gallium(III) tris(ethoxycarbonyl)corrole (1-Ga). Its in vitro PDT activities towards different cancer cell lines were examined, and the best PDT activity was observed in A549 cell lines. 1-Ga could penetrate the cell membrane rapidly and exhibit remarkable photo-cytotoxicity. 1-Ga can induce A549 cell apoptosis via ROS-mediated mitochondrial pathways, in which p38 and sirt-1 proteins play a key role. A PTD test in vivo showed that 1-Ga can significantly reduce the growth of A549 xenografted tumor cells without an obvious loss of mice weight upon PDT treatment.