Background This study aimed to identify altered exosome circular RNA (circRNA) in the serum of patients with papillary thyroid carcinoma using high-throughput sequencing. Material/Methods Serum was collected from three patients with papillary thyroid carcinoma and three patients with a benign thyroid goiter. Exosomes were isolated using an exosome isolation kit and confirmed by transmission electron microscopy. Exosome circRNAs were analyzed by high-throughput sequencing using the HiSeq 4000 sequencer. The differentially expressed circRNAs were confirmed by fluorescence quantitative real-time polymerase chain reaction (qRT-PCR). Results Twenty-two differentially expressed circRNAs were screened, which included three that were upregulated and 19 that were down-regulated in serum from patients with papillary thyroid carcinoma compared with controls. Gene Ontology (GO) enrichment analysis showed that these differentially expressed circRNAs were associated with 16 signaling pathways, including the thyroid hormone signaling pathway, the PI3K-Akt signaling pathway, and the AMPK signaling pathway. Three differentially regulated circRNAs included hsacirc_007293, hsacirc_031752, and hsacirc_020135 were confirmed by qRT-PCR. The expression trends were consistent between the high-throughput sequencing technique and qRT-PCR. Conclusions The findings from this study have shown that gene regulation can be studied from exosomes obtained from serum samples in patients with papillary thyroid carcinoma, and supports the need for further studies on the role of exosome circRNAs in thyroid cancer.
Myocardial ischemia/reperfusion injury often leads to adverse cardiovascular outcomes due to severe hypoxia. The present study aimed to evaluate the effects and mechanism of long non-coding rna H19 (H19) on rat H9c2 cells with hypoxia-induced injury. H9c2 cells were infected with lentiviruses to express H19 or H19-targeting short hairpin rna (shrna), or their respective controls, at a multiplicity of infection of 1:100. H19 expression was determined by reverse transcription-quantitative Pcr. Hypoxic injury was induced and assessed by analyzing the level of apoptosis, the cell cycle distribution and the mitochondrial membrane potential using flow cytometry in the different groups. The expression of the Pi3K/aKT and the erK/p38 signaling pathways were analyzed using western blotting. it was found that hypoxia stimulated apoptosis, induced G1 phase cell cycle arrest and increased the mitochondrial depolarization rate in H9c2 cells. When compared with the hypoxic model group, the H19 overexpression group had a significantly reduced rate of apoptosis (P=0.016), a smaller G1 population and a higher S phase population (P=0.018 and P=0.031, respectively), and a reduced mitochondrial depolarization rate (P=0.036). By contrast, the H19 shrna group exhibited the opposite trends, suggesting that hypoxia-induced injury was alleviated by the overexpression of H19 and was aggravated by the knockdown of H19. The present mechanistic studies revealed that H19 may decrease hypoxia-induced cell injury by activating the Pi3K/aKT and erK/p38 pathways. The results of the present study suggested that H19 may alleviate hypoxia-induced myocardial cell injury through the activation of the Pi3K/aKT and erK/p38 pathways.
Accumulated evidences suggested that circular RNAs (circRNA) played critical roles in tumorigenesis and progression. To our knowledge, no study reported the function of circular RNA DGKB (circDGKB, circRNA ID: hsa_circ_0133622) on progression of neuroblastoma (NB). Here, we showed that circDGKB was upregulated in NB tissues compared to the normal dorsal root ganglia. Moreover, the expression level of circDGKB was negatively correlated with the survival rate of NB patients. Mechanically, overexpression of circDGKB promoted the proliferation, migration, invasion, and tumorigenesis of NB cells and reduced cell apoptosis, and vice versa. In addition, qRT-PCR and/or Western blot results showed that circDGKB overexpression inhibited the expression level of miR-873 and enhanced GLI1 expression. Moreover, miR-873 functioned an opposite role to circDGKB and significantly weakened circDGKB role in promoting NB progression. Furthermore, GLI1 upregulation also rescued the miR-873 role in inhibiting NB progression. In conclusion, our work proved that circDGKB promoted NB progression via targeting miR-873/GLI1 axis in vitro and in vivo. Our study provided a new target for NB treatment and indicated that circDGKB could act as a novel diagnostic marker for NB.
In order to solve the problem that the traditional DWA algorithm cannot have both safety and speed because of the fixed parameters in the complex environment with many obstacles, a parameter adaptive DWA algorithm (PA-DWA) is proposed to improve the robot running speed on the premise of ensuring safety. Firstly, the velocity sampling space is optimized by the current pose of the mobile robot, and a criterion of environment complexity is proposed. Secondly, a parameter-adaptive method is presented to optimize the trajectory evaluation function. When the environment complexity is greater than a certain threshold, the minimum distance between the mobile robot and the obstacle is taken as the input, and the weight of the velocity parameter is adjusted according to the real-time obstacle information dynamically. The current velocity of the mobile robot is used as input to dynamically adjust the weight of the direction angle parameter. In the Matlab simulation, the total time consumption of PA-DWA is reduced by 47.08% in the static obstacle environment and 39.09% in the dynamic obstacle environment. In Gazebo physical simulation experiment, the total time of PA-DWA was reduced by 26.63% in the case of dynamic obstacles. The experimental results show that PA-DWA can significantly reduce the total time of the robot under the premise of ensuring safety.
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