Background Currently, the prognosis of non‐small‐cell lung cancer (NSCLC) patients remains dismal due to recurrence and metastasis. The purpose of our study was to explore the role of circular RNA_0016760 (circ_0016760) in NSCLC progression and its associated mechanism. Methods Quantitative real‐time polymerase chain reaction (qRT‐PCR) was implemented to measure the expression of circ_0016760, microRNA‐646 (miR‐646) and AK strain thymoma serine/threonine kinase 3 (AKT3). The protein level of AKT3 was examined by Western blot assay. Cell Counting Kit 8 assay, transwell assays, and flow cytometry were conducted to analyze cell proliferation, metastasis, and apoptosis. Dual‐luciferase reporter assay was used to confirm the interactions that were predicted by bioinformatics software (Circular RNA Interactome and TargetScan). A xenograft tumor model was built to investigate the role of circ_0016760 in vivo. Results Circ_0016760 and AKT3 were highly expressed in NSCLC tissue specimens and cell lines. Circ_0016760 interference suppressed cell proliferation, migration, and invasion and promoted the apoptosis of NSCLC cells. Circ_0016760 interacted with miR‐646 and negatively regulated its expression. MiR‐646 silencing partly counteracted circ_0016760 knockdown‐mediated influences in NSCLC cells. MiR‐646 bound to the AKT3 3′ untranslated region in NSCLC cells, and miR‐646 overexpression‐induced effects in NSCLC cells were partly overturned by the addition of AKT3 overexpression plasmid. Circ_0016760 silencing reduced the expression of AKT3 through enhancing miR‐646 expression. Circ_0016760 knockdown suppressed NSCLC tumor growth in vivo. Conclusion Circ_0016760 played an oncogenic role to promote the proliferation, migration, and invasion and restrained the apoptosis of NSCLC cells via miR‐646/AKT3 signaling.
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Background: Cerebral infarction associated with atrial fibrillation (AF) has relatively higher mortality and morbidity rates than other types of stroke. Statins are being commonly prescribed to patients with stoke. However, the use of statins in AF-related stroke, especially prestroke, has not been well studied. This study aimed to investigate whether the use of prestroke statins could improve clinical outcomes in patients with AF-related acute ischemic stroke (AIS) and its mechanism. Methods: This prospective study enrolled 453 AF-associated AIS patients from 4 medical centers and divided them into 2 groups based on the statin use before the stroke episode. All patients received comprehensive clinical examinations including 72-h Holter electrocardiogram monitoring and were followed up for 3 months. Plasma suppressor of cytokine signaling-3 (SOCS-3) and matrix metalloproteinase-9 (MMP-9) levels were measured by ELISA on admission and days 3 and 7 after enrollment. The endpoints were death, major disability (modified Rankin Scale score ≥3), and composite outcome (death/major disability) at 3 months after the AIS episode. Results: Plasma SOCS-3 levels were significantly increased and MMP-9 levels decreased in patients in the prestroke statin group on hospital admission and days 3 and 7 after enrollment (p < 0.001). Furthermore, our data suggested that baseline plasma SOCS-3 levels were associated with increased risk of 3-month mortality (adjusted odds ratio [OR], 1.012; 95% confidence interval [CI], 1.006–1.018; p < 0.001) and major disability (adjusted OR, 1.013; 95% CI, 1.007–1.02; p < 0.001). Similarly, baseline plasma MMP-9 levels were also associated with increased risk of 3-month mortality (adjusted OR, 1.037; 95% CI, 1.022–1.053; p < 0.001) and major disability (adjusted OR, 1.038; 95% CI, 1.022–1.55; p < 0.001). Conclusion: Our data suggested that the prestroke use of statins improved the clinical outcomes in AIS patients with AF by upregulating the level of SOCS-3 and reducing the plasma MMP-9 level.
Introduction: Endovascular therapy (EVT) for intracranial arterial aneurysms is depicted with several complications. Very recently, delayed non-ischemic cerebral enhanced (NICE) lesions have been identified as a rare complication associated with EVT. This complication always stands a higher chance of being missed in asymptomatic patients. We report a case of multiple NICE lesions in a known chronic hepatitis B infection and chronic gastritis patient with left internal carotid aneurysm (ICA) treated with detachable coils. Case Presentation: A 52 years old female with left ICA was treated with detachable coils via the endovascular route. Three weeks after the operation, she presented with numbness of her right limbs which was persistent and waked her up from sleep each night. She admitted skin allergies after wearing metals except for gold and silver since childhood. MRI revealed multiple abnormal lesions in the left temporal lobe, hippocampus, insula, and parietal lobe and some perifocal edema which were consistent with the diagnosis of delayed NICE lesions. Conclusion: It is very important to report the occurrences of these lesions in literature because of their allergic origin. We advocate that allergy to metals especially those used in coating endovascular equipment should be evaluated before every EVT for intracranial aneurysms.
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