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The universal flexoelectric effect in solids provides a mechanical pathway for controlling electric polarization in ultrathin ferroelectrics, eliminating potential material breakdown from a giant electric field at the nanoscale. One challenge of this approach is arbitrary implementation, which is strongly hindered by one-way switching capability. Here, utilizing the innate flexibility of van der Waals materials, we demonstrate that ferroelectric polarization and domain structures can be mechanically, reversibly, and arbitrarily switched in two-dimensional CuInP2S6 via the nano-tip imprinting technique. The bidirectional flexoelectric control is attributed to the extended tip-induced deformation in two-dimensional systems with innate flexibility at the atomic scale. By employing an elastic substrate, artificial ferroelectric nanodomains with lateral sizes as small as ~80 nm are noninvasively generated in an area of 1 μm2, equal to a density of 31.4 Gbit/in2. Our results highlight the potential applications of van der Waals ferroelectrics in data storage and flexoelectronics. Flexoelectric effect may offer a voltage-free method to control the polarization in 2D ferroelectrics, but its widespread application remains challenging. Here, the authors report an approach to arbitrarily switch the ferroelectricity in 2D CuInP2S6. [ABSTRACT FROM AUTHOR]

The role of ATP6AP1 in colorectal cancer (CRC) remains elusive despite its observed upregulation in pan-cancer. Therefore, the current study aimed to assess the clinical significance of ATP6AP1 and its relationship with the immune infiltration in CRC. Transcriptome data of CRC were obtained from The Cancer Genome Atlas (TCGA) database and analyzed using the combination of R packages and tumor-related databases, including TIMER2, TISIDB, cBioPortal, and MethSurv. The tissue arrays and immunohistochemical staining were performed to verify the expression and clinical characteristics of ATP6AP1. The results revealed that ATP6AP1 expression was significantly elevated in CRC and associated with poor clinicopathological characteristics and prognosis. Furthermore, the analysis demonstrated ATP6AP1 expression was correlated with the infiltration of immune cells and cancer-associated fibroblasts in the microenvironment of CRC. Moreover, ATP6AP1 was found to be linked to various immune checkpoints and chemokines, with enrichment of cytoplasmic vesicle lumen, endopeptidase regulator activity, and endopeptidase inhibitor activity observed in the high ATP6AP1 expressional group. In conclusion, the findings of this study suggest that ATP6AP1 upregulation may serve as a biomarker for poor diagnosis in CRC and offer a potential target for immunotherapy in CRC. [ABSTRACT FROM AUTHOR]