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Ferroptosis is a newly-discovered cell death mechanism involved in the progression of various tumors, the role of noncoding RNAs (ncRNAs) in it was relatively less explored. This study identified the low levels of a recently studied long noncoding RNA (lncRNA), A2M-AS1, in pancreatic cancer and suggested its positive correlation with the overall survival time of patients with pancreatic cancer. A2M-AS1 was mainly localized in the cytoplasm, inhibiting the cellular proliferation, migration, and invasion as well as the tumor growth of the pancreatic cancer cells. Moreover, the Erastin-induced ferroptosis increased the expression levels of A2M-AS1. The overexpression of A2M-AS1 promoted ferroptosis in the pancreatic cancer, which was inhibited by the silencing of A2M-AS1. Mechanically, A2M-AS1 could directly interact with the poly (rC) binding protein 3 (PCBP3), which plays an important role in the process of iron metabolism, thereby promoting the ferroptosis in pancreatic cancer. In addition, the A2M-AS1/PCBP3 axis could facilitate the p38 activation and inhibit the phosphorylation of the AKT–mTOR signaling pathway; all these participate in regulating ferroptosis. In conclusion, the regulation of ferroptosis by targeting the A2M-AS1/PCBP3 axis might provide a novel target for the treatment of pancreatic cancer in the future. Implications: A2M-AS1 might be a potential novel therapeutic target for patients with pancreatic cancer in the future.

Supplementary Table from LncRNA A2M-AS1 Promotes Ferroptosis in Pancreatic Cancer via Interacting With PCBP3

Supplementary Figure from LncRNA A2M-AS1 Promotes Ferroptosis in Pancreatic Cancer via Interacting With PCBP3

Pancreatic cancer is one of the malignant tumors with the worst prognosis, and the 5-year survival rate of this disease is less than 1%. About 90% of pancreatic cancer is pancreatic ductal adenocarcinoma (PDAC), and targeting therapy has become a promising treatment for PDAC in recent years. To improve the survival rate, novel therapeutic targets for PDAC are still urgently needed. KIF18B was initially identified as a member of the kinesin family and involved in multiple cellular processes, such as separation of chromosomes in mitosis. Recently, it was found that KIF18B was involved in the growth and development of multiple cancers. However, the potential link between KIF18B and PDAC is still unclear. In this study, we demonstrated that KIF18B was highly expressed in human PDAC tissues, and related with the poor prognosis and clinical features, such as tumor size (*p = .013) and pTNM stage (*p = .025), of patients with PDAC. We further found that KIF18B knockdown blocked the cell proliferation of PDAC in vitro and in vivo, and the cell cycle was arrested caused by KIF18B depletion. Additionally, we also found that KIF18B bound to the promoter region of the cell division cycle associated 8 and thus activated its transcription. Taken together, this study explored the molecular mechanism underlying KIF18B promoting PDAC and provided a novel therapeutic target of this disease.

We review machine learning and its applications ina wide range of electromagnetic problems, including radar,communication, imaging and sensing. We extensively discuss some recent progress in development and use of intelligent algorithms for antenna design, synthesis, and characterization. We also provide some perspectives for future research directions in this emerging field of study.

Foodborne pathogens can survive as the state of sublethal injury in adverse environments and recover physiological function and virulence under suitable conditions. Slightly acidic electrolyzed water (SAEW) is a non-thermal treatment to decontaminate in food industry and can induce sublethal injury. However, sublethal injury induced by SAEW and recoveries of different pathogens have not been fully investigated. In this study, it was observed that sublethally injured L. monocytogenes and E. coli O157:H7 cells widely persisted after exposure to different SAEW treatments (both of two pathogens: volumes of SAEW 1–10 ml, concentrations of SAEW 25%–100%; L. monocytogenes: treatment time 30–180 s, E. coli O157:H7: treatment time 15–90 s). And the highest recovery ratio of injured L. monocytogenes or E. coli O157:H7 was observed in TSB-YE or TSB and these cells were completely recovered within 60 min or 2.5 h, respectively. The recovery ratio of SAEW-injured L. monocytogenes and E. coli O157:H7 increased as recovery temperature increasing (4–37 °C). Mg, Ca and Zn cations significantly improved the recovery ratios of both two pathogens, but Fe and Mn cations had negative effects on recovery. Moreover, the concentrations of cations (0.5–8 mM) affected repair. The most appropriate concentration of Mg, Ca or Zn cations improving the repair of injured L. monocytogenes was 1 mM, 8 mM or 0.5 mM, respectively. The recovery ratio of injured E. coli O157:H7 increased with the concentrations of Mg, Ca and Zn cations increasing. The understanding of SAEW-injured and resuscitated conditions of L. monocytogenes and E. coli O157:H7 can avoid the occurrence of injured cells in food processing and develop a medium for detecting injured pathogens.