BackgroundGastric cancer receives considerable attention not only because it is the most common cancer all through the world, but also because it’s on the top third leading reason for cancer-related death. Lidocaine is a well-documented local anesthetic that has been reported to suppress cancer development. The study explored the effects of lidocaine on the growth, migration and invasion of the gastric carcinoma cell line MKN45 and the mechanism behind.MethodsThe effect of lidocaine on viability, proliferation and apoptosis of MKN45 cells were analyzed by Cell Counting Kit-8 assay, BrdU staining assay and flow cytometry, respectively. Moreover, cell migration and invasion were both examined by Transwell assay. The expression of apoptosis-, migration-, and invasion-related proteins were detected by western blot. The relative expression of miR-145 was determined by qRT-PCR. Moreover, the impact which lidocaine brought on MEK/ERK and NF-κB pathways were examined by western blot.ResultsLidocaine inhibited viability, proliferation, migration, and invasion of MKN45 cells, while enhanced apoptosis. Moreover, miR-145 expression was enhanced by lidocaine; and transfection with miR-145 inhibitor increased cell viability, proliferation, migration, and invasion, but inhibited apoptosis. The up-regulation of miR-145 was partly contributed to the inhibitory effect of lidocaine on gastric cancer cell line MKN45. Finally, lidocaine inactivated MEK/ERK and NF-κB pathways via up-regulation of miR-145.ConclusionsOur results suggested that lidocaine decreased growth, migration and invasion of MKN45 cells via regulating miR-145 expression and further inactivation of MEK/ERK and NF-κB signaling pathways.
Propofol is frequently used for anesthesia in cancer surgery. It has been suggested that treatment with propofol serves a tumor-suppressing role in human gastric cancer (GC). Therefore, the present study aimed to explore the potential mechanism of propofol in GC. In the present study, GC cell lines (HGC-27 and AGS) were treated with various concentrations of propofol, and an MTT assay was performed to detect the cell viability. In addition, flow cytometry and Transwell assays were used to evaluate the apoptosis and invasive ability of GC cells, respectively. Western blotting was performed to detect the protein levels of cyclin-dependent kinase inhibitor P21 (P21), B-cell lymphoma-2 (Bcl-2), matrix metalloproteinase 9 (MMP9) and E26 oncogene homolog 1 (ETS1). Furthermore, reverse transcription-quantitative PCR was used to examine the expression levels of circular RNA-PVT1 (circ-PVT1), ) and ETS1 in GC tissues and cells. The target interaction between miR-195-5p and circ-PVT1 or ETS1 was predicted through bioinformatics analysis, and verified by dual-luciferase reporter gene assay. In addition, a mouse xenograft model was established for in vivo experiments. It was identified that propofol inhibited the viability and invasion, but promoted apoptosis of HGC-27 and AGS cells in a dose-dependent manner. Propofol could inhibit Bcl-2 and MMP9 expression, and increase P21 expression in GC cells. The expression levels of circ-PVT1 and ETS1 were increased in GC tissues and cells, and miR-195-5p was decreased. Additionally, the treatment with propofol could lead to decreased circ-PVT1 expression in GC cells. These results could be reversed by ETS1 upregulation or miR-195-5p-knockdown in GC cells. Furthermore, circ-PVT1 could act as a miR-195-5p sponge to modulate ETS1 expression. Additionally, the effects of transfection with circ-PVT1 small interfering RNA (si-circ-PVT1) on HGC-27 and AGS cells could be reversed by treatment with miR-195-5p inhibitor. Meanwhile, miR-195-5p inhibitor reversed the si-circ-PVT1-induced low expression of ETS1. Downregulation of ETS1 induced by propofol in HGC-27 and AGS cells could be restored by circ-PVT1 upregulation or miR-195-5p silencing. Circ-PVT1 silencing facilitated the propofol-induced anti-GC effect in vivo. In conclusion, the present study indicated that propofol inhibited the proliferation and invasion, but enhanced the apoptosis of GC cells by regulating the circ-PVT1/miR-195-5p/ETS1 axis.
Steam methane reforming is a major method of hydrogen production. However, this method usually suffers from low energy efficiency and high carbon-emission intensity. To solve this issue, a novel steam-methane-reforming process over a Ni-based catalyst in a pressurized dual fluidized bed reactor is proposed in this work. A three-dimensional computational fluid dynamics (CFD) model for the complex physicochemical process was built to study the reforming characteristics. The model was first validated against the reported data in terms of hydrodynamics and reaction kinetics. Next, the performance of the proposed methane-steam-reforming process was predicted. It was found that the methane-conversion ratio was close to 100%. The mole fraction of H2 in the dry-yield syngas reached 98.8%, the cold gas efficiency reached 98.5%, and the carbon-capture rate reached 96.4%. It is believed that the proposed method can be used for methane reforming with high efficiency and low carbon intensity.
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