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Emerging high entropy compounds (HECs) have attracted huge attention in electrochemical energy‐related applications. The features of ultrafine size and carbon incorporation show great potential to boost the ion‐storage kinetics of HECs. However, they are rarely reported because high‐temperature calcination tends to result in larger crystallites, phase separation, and carbon reduction. Herein, using the NaCl self‐assembly template method, by introducing a high‐pressure field in the calcination process, the atom diffusion and phase separation are inhibited for the general formation of HECs, and the HEC aggregation is inhibited for obtaining ultrafine size. The general preparation of ultrafine‐sized (<10 nm) HECs (nitrides, oxides, sulfides, and phosphates) anchored on porous carbon composites is realized. They are demonstrated by combining advanced characterization technologies with theoretical computations. Ultrafine‐sized high entropy sulfides‐MnFeCoCuSnMo/porous carbon (HES‐MnFeCoCuSnMo/PC) as representative anodes exhibit excellent sodium‐ion storage kinetics and capacities (a high rating capacity of 278 mAh g−1 at 10 A g−1 for full cell and a high cycling capacity of 281 mAh g−1 at 20 A g−1 after 6000 cycles for half cell) due to the combining advantages of high entropy effect, ultrafine size, and PC incorporation. Our work provides a new opportunity for designing and fabricating ultrafine‐sized HECs. [ABSTRACT FROM AUTHOR]

Recently, long noncoding RNAs (lncRNAs) have become the key gene regulators and prognostic biomarkers in various cancers. Through microarray data, Linc00339 was identified as a candidate oncogenic lncRNA. We compared the expression levels of Linc00339 in several breast cancer cell lines and normal mammary gland epithelial cell line. The effects of Linc00339 on tumor progression were examined both in vitro and in vivo. 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assays were applied to evaluate the functions of Linc00339, miR‐377‐3p, and HOXC6 on cell proliferation. Flow cytometry analysis was used to detect apoptosis and cell cycle distribution. Overall survival (OS) was analyzed using data from The Cancer Genome Atlas and molecular taxonomy of breast cancer international consortium (METABRIC). Dual luciferase assay and RNA immunoprecipitation were performed to confirm the interaction between Linc003339 and miR‐377‐3p. Linc00339 was increased in breast cancer cell lines compared with the normal epithelial cell. Through in vitro and in vivo experiments, Linc00339 overexpression promoted triple‐negative breast cancer (TNBC) proliferation, inhibited cell cycle arrest, and suppressed apoptosis. Silencing of Linc00339 obtained the opposite effects. Mechanistic investigations demonstrated that Linc00339 could sponge miR‐377‐3p and regulate its expression. Higher expression of miR‐377‐3p indicated longer OS in breast cancer patients, especially in TNBC patients. Overexpression of miR‐377‐3p retarded TNBC cell growth through regulating cell cycle distribution and apoptosis. And miR‐377‐3p was involved in Linc00339‐mediated TNBC proliferation through regulating HOXC6 expression. Knockdown of HOXC6 inhibited TNBC progression. In conclusion, our results illuminated that the novel Linc00339/miR‐377‐3p/HOXC6 axis played a critical role in TNBC progression and might be a promising therapeutic target for TNBC treatment. [ABSTRACT FROM AUTHOR]