11 research outputs found

    Sevoflurane suppresses the malignant progression of breast cancer via the hsa_circ_0000129/miR‐578/EPSTI1 axis

    No full text
    Abstract Background Sevoflurane (Sev) is a commonly used volatile anesthetic that might suppress the process of breast cancer. Also, circular RNAs (circRNAs) have been reported to partake in the pathogenesis of breast cancer. Accordingly, this research was designed to investigate the mechanism of hsa_circ_0005962 on Sev‐mediated breast cancer development. Methods Sev was applied to treat breast cancer cells. Cell proliferation ability, migration, invasion, and apoptosis were detected using Cell Counting Kit‐8 (CCK‐8), 5‐ethynyl‐2′‐deoxyuridine (EdU), Transwell, and flow cytometry assay. Proliferating cell nuclear antigen (PCNA), Matrix metallopeptidase 9 (MMP9), B‐cell lymphoma‐2 (Bcl‐2)‐associated X protein (Bax), and Epithelial stromal interaction 1 (EPSTI1) were assessed using western blot assay. circ_0000129, microRNA‐578 (miR‐578), and EPSTI1 levels were determined using real‐time quantitative polymerase chain reaction (RT‐qPCR). Using bioinformatics software (Circinteractome and Targetscan), the binding between miR‐578 and circ_0000129 or EPSTI1 were predicted, and proved using dual‐luciferase reporter and RNA pull‐down assay. The biological roles of circ_0000129 and Sevoflurane on tumor growth were analyzed using a xenograft tumor model in vivo. Results Sevoflurane blocked tumor cell proliferation, migration, invasion, and promoted apoptosis. Circ_0000129 and EPSTI1 expression were increased, and miR‐578 was decreased in breast cancer cells. Also, they presented an opposite trend in Sev‐treated tumor cells. Circ_0000129 upregulation might abolish Sev‐mediated tumor progression in vitro. Mechanically, circ_0000129 can affect EPSTI1 expression by sponging miR‐578. Sev might inhibit tumor growth by regulating circ_0000129 in vivo. Conclusion Circ_0000129 relieved Sev‐triggered suppression impacts on breast cancer development partly via the miR‐578/EPSTI1 axis, which provides a new mechanism for studying mediated therapy of breast cancer treatment

    Mobility Enhancement of Strained MoS<sub>2</sub> Transistor on Flat Substrate

    No full text
    Strain engineering has been proposed as a promising method to boost the carrier mobility of two-dimensional (2D) semiconductors. However, state-of-the-art straining approaches are largely based on putting 2D semiconductors on flexible substrates or rough substrate with nanostructures (e.g., nanoparticles, nanorods, ripples), where the observed mobility change is not only dependent on channel strain but could be impacted by the change of dielectric environment as well as rough interface scattering. Therefore, it remains an open question whether the pure lattice strain could improve the carrier mobilities of 2D semiconductors, limiting the achievement of high-performance 2D transistors. Here, we report a strain engineering approach to fabricate highly strained MoS2 transistors on a flat substrate. By mechanically laminating a prefabricated MoS2 transistor onto a custom-designed trench structure on flat substrate, well-controlled strain can be uniformly generated across the 2D channel. In the meantime, the substrate and the back-gate dielectric layer remain flat without any roughness-induced scattering effect or variation of the dielectric environment. Based on this technique, we demonstrate the MoS2 electron mobility could be enhanced by tension strain and decreased by compression strain, consistent with theoretical predictions. The highest mobility enhancement is 152% for monolayer MoS2 and 64% for bilayer MoS2 transistors, comparable to that of a silicon device. Our method not only provides a compatible approach to uniformly strain the layered semiconductors on flat and solid substrate but also demonstrates an effective method to boost the carrier mobilities of 2D transistors
    corecore