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Ferroptosis is a newly discovered iron-dependent form of regulated cell death driven by phospholipid peroxidation and associated with processes including iron overload, lipid peroxidation, and dysfunction of cellular antioxidant systems. Ferroptosis is found to be closely related to many diseases, including cancer at every stage. Epithelial–mesenchymal transition (EMT) in malignant tumors that originate from epithelia promotes cancer-cell migration, invasion, and metastasis by disrupting cell–cell and cell–cell matrix junctions, cell polarity, etc. Recent studies have shown that ferroptosis appears to share multiple initiators and overlapping pathways with EMT in cancers and identify ferroptosis as a potential predictor of various cancer grades and prognoses. Cancer metastasis involves multiple steps, including local invasion of cancer cells, intravasation, survival in circulation, arrest at a distant organ site, extravasation and adaptation to foreign tissue microenvironments, angiogenesis, and the formation of "premetastatic niche". Numerous studies have revealed that ferroptosis is closely associated with cancer metastasis. From the cellular perspective, ferroptosis has been implicated in the regulation of cancer metastasis. From the molecular perspective, the signaling pathways activated during the two events interweave. This review briefly introduces the mechanisms of ferroptosis and discusses how ferroptosis is involved in cancer progression, including EMT, cancer angiogenesis, invasion, and metastasis. [ABSTRACT FROM AUTHOR]

Recently, although aqueous zinc ion batteries have caused widespread concerns, the pieces of research on new anode materials are still very limited. And herein, monoclinic MoOx anode material with impressive properties for rechargeable aqueous zinc ion batteries is synthesized by a facile N-methylpyrrolidone-assisted wet-chemical method for the first time. The monoclinic MoOx anode material delivers high initial discharge/charge capacities of 233.7/203.7 mAh g−1 at a current density of 0.5 A g−1. What is more, even at an extremely high current density of 20 A g−1, high initial discharge/charge capacities of 173.3/122.2 mAh g−1 can be still exhibited, and the highest charge capacity of 145.0 mAh g−1, which corresponds to a discharge capacity of 146.7 mAh g−1 is delivered at the 8th cycle. Furthermore, the anode material could still work effectively even after 40,000 cycles at 20 A g−1 that considerable discharge/charge capacities of 38.3/38.3 mAh g−1 can be still exhibited. The significance of the rational designing the ratio between the cathode material mass and the monoclinic MoOx anode mass is also illustrated here, and it is found the optimized cell (cathode: anode mass ratio of 2:1) exhibits great electrochemical properties enhancement including higher capacity, better rate property, and better cycle ability. [ABSTRACT FROM AUTHOR]

Objectives: YTHDF1 is known as a m6A reader protein, and many researches of YTHDF1 focused on the regulation of mRNA translation efficiency. However, YTHDF1 is also related to RNA degradation, but how YTHDF1 regulates mRNA degradation is indefinite. Liquid‐liquid phase separation (LLPS) underlies the formation of membraneless compartments in mammal cells, and there are few reports focused on the correlation of RNA degradation with LLPS. In this research, we focused on the mechanism of YTHDF1 degraded mRNA through LLPS. Materials and Methods: The CRISPR/Cas9 knock out system was used to establish the YTHDF1 knock out (YTHDF1‐KO) cell lines (HEK293 and HeLa) and METTL14 knock out (METTL14‐KO) cell line (HEK293). 4SU‐TT‐seq was used to check the half‐life changes of mRNAs. Actinomycin D and qPCR were used to test the half‐life changes of individual mRNA. RNA was stained with SYTO RNA‐select dye in wild type (WT) and YTHDF1‐KO HeLa cell lines. Co‐localization of YTHDF1 and AGO2 was identified by immunofluorescence. The interaction domain of YTHDF1 and AGO2 was identified by western blot. Phase separation of YTHDF1 was performed in vitro and in vivo. Fluorescence recovery after photobleaching (FRAP) was performed on droplets as an assessment of their liquidity. Results: In this research, we found that deletion of YTHDF1 led to massive RNA patches deposited in cytoplasm. The results of 4SU‐TT‐seq showed that deletion of YTHDF1 would prolong the half‐life of mRNAs. Immunofluorescence data showed that YTHDF1 and AGO2 could co‐localize in P‐body, and Co‐IP results showed that YTHDF1 could interact with AGO2 through YT521‐B homology (YTH) domain. We confirmed that YTHDF1 could undergo phase separation in vitro and in vivo, and compared with AGO2, YTHDF1 was more important in P‐body formation. The FRAP results showed that liquid AGO2 droplets would convert to gel/solid when YTHDF1 was deleted. As AGO2 plays important roles in miRISCs, we also found that miRNA‐mediate mRNA degradation is related to YTHDF1. Conclusions: YTHDF1 recruits AGO2 through the YTH domain. YTHDF1 degrades targeting mRNAs by promoting P‐body formation through LLPS. The deletion of YTHDF1 causes the P‐body to change from liquid droplets to gel/solid droplets, and form AGO2/RNA patches, resulting in a degradation delay of mRNAs. These findings reveal a previously unrecognized crosstalk between YTHDF1 and AGO2, raising a new sight of mRNA post‐transcriptional regulation by YTHDF1. [ABSTRACT FROM AUTHOR]