Developing highly active nonprecious electrocatalysts with superior durability for both the hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) is crucial to improve the efficiency of overall water splitting but remains challenging. Here, a novel superhydrophilic Co4N‐CeO2 hybrid nanosheet array is synthesized on a graphite plate (Co4N‐CeO2/GP) by an anion intercalation enhanced electrodeposition method, followed by high‐temperature nitridation. Doping CeO2 into Co4N can favor dissociation of H2O and adsorption of hydrogen, reduce the energy barrier of intermediate reactions of OER, and improve the compositional stability, thereby dramatically boosting the HER performance while simultaneously inducing enhanced OER activity. Furthermore, the superhydrophilic self‐supported electrode with Co4N‐CeO2 in situ grown on the conductive substrate expedites electron conduction between substrate and catalyst, promotes the bubble release from electrode timely and impedes catalyst shedding, ensuring a high efficiency and stable working state. Consequently, the Co4N‐CeO2/GP electrode shows exceptionally low overpotentials of 24 and 239 mV at 10 mA cm−2 for HER and OER, respectively. An alkaline electrolyzer by using Co4N‐CeO2/GP as both the cathode and anode requires a cell voltage of 1.507 V to drive 10 mA cm−2, outperforming the Pt/C||RuO2 electrolyzer (1.540 V@10 mA cm−2). More significantly, the electrolyzer has extraordinary long‐term durability at a large current density of 500 mA cm−2 for 50 h, revealing its potential in large‐scale applications.

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MicroRNAs (miRNAs) present frequently altered expression in urologic cancers including prostate, bladder, and kidney cancer. The altered expression of miR-223 has been reported in cancers and other diseases in recent researches. MiR-223 is up-regulated in systemic lupus erythematosus and rheumatoid arthritis. In neoplastic diseases, miR-223 is proved to be up-expressed in plasma or serum and cancer tissues compared with normal tissues in pancreatic cancer, gastric cancer, et al. However, whether altered expression of miR-223 is associated with prostate cancer (PCa) and what it is potential functions in PCa remained unveiled. In this study, we firstly found miR-223-3p were up-regulated in prostate cancer tissues and then we study functional role of miR-223-3p in PCa using DU145, PC3 and LNCaP cell lines. Our data suggested that miR-223-3p might target gene SEPT6 and promoted the biological behavior of prostate cancer. Notably, we found increasing SEPT6 expression might reverse the biological activity induced by miR-223-3p, which might be a potential therapeutic target for PCa.

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