Browsing by Subject "Propofol"

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    Anesthetic propofol suppresses growth and metastasis of lung adenocarcinoma in vitro through downregulating circ-MEMO1-miR-485-3p-NEK4 ceRNA axis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Chen, Lei; Wu, Guangyi; Li, Yongle; Cai, Qiaoying
    Background. Recently, circular RNAs (circRNAs) have been emerging as new regulators in the propofol-induced tumor-suppressive role. Here, we intended to investigate the involvement of circRNAMediator of cell motility 1 (circ-MEMO1; hsa_circ_0007385) in propofol role in cancer hallmarks of lung adenocarcinoma (LUAD). Methods. Real-time quantitative PCR and western blotting examined transcriptional and translational levels of circ-MEMO1, microRNA (miR)-485-3p, and NIMArelated kinase-4 (NEK4), and markers of growth and metastasis including E-cadherin, CyclinD1, and Vimentin. Cancer hallmarks were measured by 3-(4, 5- dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, 5-ethynyl-2-deoxyuridine assay, and transwell assay. The interaction among circMEMO1, miR-485-3p, NEK4 was determined by dualluciferase reporter assay and Pearson’s correlation analysis. Results. Circ-MEMO1 and NEK4 were highexpressed, and miR-485-3p was low-expressed in LUAD patients and cells; moreover, circ-MEMO1 and NEK4 expression in LUAD cells could be suppressed, whereas miR-485-3p could be elevated with propofol anesthesia. Functionally, propofol restrained cell viability, cell cycle entrance, cell proliferation, migration, and invasion of LUAD cells, accompanied by promoted E-cadherin and depressed CyclinD1 and Vimentin. Coincidently, high circ-MEMO1 was associated with low overall survival of LUAD patients, and overexpressing circ-MEMO1 could overall attenuate propofol effects in LUAD cells. Of note, upregulating miR-485-3p and/or interfering NEK4 could partially countermand the adverse impacts of circ-MEMO1 on propofol’s role in LUAD cells. Importantly, circMEMO1 acted as a sponge for miR-485-3p to modulate the expression of miR-485-3p-targeted oncogene NEK4. Conclusion. Promoting the circ-MEMO1-miR-485- 3p-NEK4 axis might halt the tumor-inhibiting role of propofol in LUAD cells in vitro, suggesting a potential epigenetic pathway of propofol.
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    Propofol protects PC12 cells from cobalt chloride-induced injury by mediating miR-134
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Zhou, Hong-Yi; Jiang, Fan; Cao, Zhong; Shen, Qi-Yun; Feng, Yu-Jing; Hou, Zhen-Huan
    Objective. Propofol (PRO) was reported to exert a neuroprotective effect by decreasing microRNA134 (miR-134), a brain-specific miRNA, thus, the role of PRO against cobalt chloride (CoCl 2)-induced injury in rat pheochromocytoma cells (PC12) via mediating miR134 was explored. Methods. CoCl 2-induced PC12 cells treated with PRO were transfected with or without miR-134 negative control (NC)/ inhibitor/mimic, and the following detections were then performed using cell counting kit-8 (CCK-8), Annexin V-fluorescein isothiocyanate/ propidium iodide (Annexin V-FITC/PI) and Hoechst 33258 staining. Autophagy was observed by transmission electron microscope (TEM). Mitochondrial membrane potential (MMP) was detected by Rhodamine-123 (Rh123) staining, and reactive oxygen species (ROS) by dichloro-dihydro-fluorescein diacetate (DCFH-DA) staining. Protein and gene expressions were measured by Western blotting and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), respectively. Results. PRO reversed the CoCl 2-induced decrease in the PC12 cell viability and increased miR-134 in a dose-dependent manner. CoCl 2 increased LC3II/I ratio and Beclin-1 expression, but decreased p62 expression, which was abolished by PRO. In addition, an increased cell apoptosis rates triggered by CoCl 2 were reduced by PRO with the down-regulations of Bax and Caspase-3 and the up-regulation of Bcl-2. Furthermore, PRO decreased methylenedioxyamphetamine (MDA), nitric oxide (NO) and ROS in CoCl 2-induced PC12 cells accompanying the increase in glutathione peroxidase (GSH-Px) and MMP. The effects of PRO on autophagy, apoptosis and oxidative stress in CoCl 2-induced PC12 cell were reversed by miR-134 mimic. Conclusion. PRO may mitigate CoCl2-induced autophagy in PC12 cells with decreased apoptosis and improved oxidative stress via mediating miR-134.