Multivalent metal ion (Mg2+, Zn2+, Ca2+, and Al3+) batteries (MMIBs) emerged as promising technologies for large-scale energy storage systems in recent years due to the abundant metal reserves in the Earth’s crust and potentially low cost. However, the lack of high-performance electrode materials is still the main obstacle to the development of MMIBs. As a newly large family of two-dimensional transition metal carbides, nitrides, and carbonitrides, MXenes have attracted growing focus in the energy storage field because of their large specific surface area, excellent conductivity, tunable interlayer spaces, and compositional diversity. In particular, the multifunctional chemistry and superior hydrophilicity enable MXenes to serve not only as electrode materials but also as important functional components for heterojunction composite electrodes. Herein, the advances of MXene-based materials since its discovery for MMIBs are summarized, with an emphasis on the rational design and controllable synthesis of MXenes. More importantly, the fundamental understanding of the relationship between the morphology, structure, and function of MXenes is highlighted. Finally, the existing challenges and future research directions on MXene-based materials toward MMIBs application are critically discussed and prospected.

Objective: The actin binding protein Vasodilator‐stimulated phosphoprotein(VASP) has complex effects on cytoskeletal organization and cell motility, which play a positive role on tumour cells migration and invasion. Our research aim to investigate the effect of epigallocatechin gallate (EGCG), an extractent from green tea, on SGC‐7901 cells migration and invasion. Methods: The expression level of VASP in SGC‐7901 cells was detected by RT‐PCR and Western Blotting. Down regulation of VASP expression was performed with VASP siRNA transfection, while the activation of Rac1 pathway was enhanced by fMLP. Wound‐healing assay (2D assay) and transwell migration assay (3D assay) were employed to analyze invasive migration ability of SGC‐7901 cells. Results: After treated with EGCG, the expression level of VASP in SGC‐7901 cells decreased significantly at mRNA and protein level compared with control group (P<0.05). In 2D assay, the cell migration velocity was reduced by EGCG (P<0.05), accordingly the EGCG group showed lower invasion capacity than the control group in 3D assay (P<0.05).The effect of EGCG on SGC‐7901 cells migration and invasion was enhanced by VASP siRNA transfection, on the contrary decreased by fMLP. Conclusion: EGCG has a inhibitive effect on SGC‐7901 cells migration and invasion by decreasing the expression level of VASP via Rac1 pathway. (This work was supported by National Natural Sciences Foundation of China under Grant No.30770966)

Cell migration is critical to many pathophysiological processes, such as tumor invasion and metastasis. It is a complicated process that is regulated by cell‐matrix adhesions and actin cytoskeleton. We report here that Vasodilator‐stimulated phosphoprotein (VASP), which has complex effects on cytoskeletal organization and cell motility. Small interfering RNAs(siRNAs) mediate RNA interference(RNAi), providing a powerful new tool for gene silencing. Herein, we explore the effect of VASP‐siRNAs on migration of MCF‐7 cells. Three pairs of VASP‐siRNAs (942, 1002, 1024) were designed, which were transfected into MCF‐7 cells via Lipofectamine 2000. To evaluate the inhibition activity of VASP‐siRNAs, VASP expression were examined with RT‐PCR and Western blotting. In MCF‐7 cells, we observed that VASP‐942 siRNA could effectively inhibit VASP expression at mRNA and protein level with a concomitant decrease of migration significantly by a wound‐healing assay. Meanwhile, the activation of Rac1 pathway by fMLP could promote the migration of MCF‐7 cells via elevating the VASP expression level. Thus, our study showed that the knockdown of VASP contributes to the reduction of migration in MCF‐7 cells. It provided that the important role of VASP in breast tumour metastasis might be regulated through Rac1 pathway. (This work was supported by National Natural Sciences Foundation of China under Grant No.30570751)