NIMA-related expressed kinase 2 (NEK2) participates in the carcinogenesis and progression of certain types of cancer, however, its expression and roles in the development of hepatocellular carcinoma (HCC) remains unknown. Here, we found that NEK2 expression was significantly upregulated in both human HCC tissues and cell lines, and increased NEK2 expression in HCC was significantly correlated with clinical progression of HCC in patients. Knockdown of NEK2 in HCC cells inhibited HCC progression, as determined by the suppressed cell proliferation, invasion and metastasis. Furthermore, knockdown of NEK2 inhibited drug resistance of HCC cells, as shown by the promoted suppression of cell viability in 5-fluorouracil (5‑FU)‑treated HCC cells. Mechanistically, protein phosphatase 1 (PP1)/Akt and Wnt signaling activation are significantly inhibited by NEK2 knockdown, which is responsible for the HCC progression and involved in NEK2‑induced cancer cell abnormal biological behavior. Thus, enhanced NEK2 expression in HCC promotes HCC progression and drug resistance by promoting PP1/Akt and Wnt pathway activation, which may represent a new therapeutic target for HCC.

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Plexins are the primary receptors of semaphorins, and participate in the majority of intracellular pathways triggered by semaphorins, including the regulation of cell adhesion and the motility of numerous cell types. Recently, several studies have reported that plexins can significantly affect different aspects of cancer cell biology, and the aberrant expression of plexins has been observed in a wide variety of tumor types. However, the expression and role of plexin-B3 in hepatocellular carcinoma (HCC) is yet to be investigated. In the present study, plexin-B3 expression was measured in 14 paired HCC samples and the corresponding adjacent non-cancerous tissue by quantitative polymerase chain reaction and western blot analysis. The results indicated that the mRNA and protein expression levels of plexin-B3 were downregulated in HCC samples when compared with the corresponding adjacent non-cancerous tissue. In order to elucidate the correlation between clinicopathological data and the expression of plexin-B3 in patients with HCC, 84 HCC archived specimens were analyzed by immunohistochemistry (IHC). The IHC results revealed that the protein expression level of plexin-B3 was lower in the HCC samples compared with the corresponding adjacent non-cancerous tissue, and plexin-B3 underexpression was correlated with the patient gender and tumor size. In conclusion, these results indicated that loss of plexin-B3 in HCC may be of predictive value for the occurrence and progression of HCC. Thus, plexin-B3 may be a promising biomarker for the diagnosis and treatment of tumors in the future.

BackgroundVenous air embolism (VAE) is a life-threatening event characterized as a series of clinical features of the disease caused by gas entering the venous circulation in the body.Case presentationA 72-year-old male patient with an ankle fracture after trauma was admitted, and complained of chest pain and dyspnea after the ankle fracture resection and internal fixation. His heart rate and blood pressure dropped, and the patient was diagnosed with VAE according to a chest x-ray and clinical features. Cardiopulmonary resuscitation was carried out and the patient's heartbeat recovered; his blood pressure rose to a normal level. The patient was still unconscious and sent to the intensive care unit for continued monitoring and treatment. Unfortunately, the patient discharged himself from the hospital and died 24 h later.ConclusionThis case suggests that x-ray may be a potential method for the rapid diagnosis of VAE in a resource-limited setting.

MicroRNAs (miRNAs) are involved in the regulation of multiple cellular pathways and play a key role in the development and progression of tumor. Based on the cellular function of their targets, miRNAs play the role of oncogenes or tumor suppressor genes. Multiple studies have shown that abnormal expression of miRNAs has close relation with the incidence of HCC, but the mechanism of miRNAs in HCC still needs further research. In the present study, we showed that the overexpression of miR-224 can reduce the mRNA and protein expression of ADAM17 and HOXA5, the silencing of miR-224 can increase the protein expression of ADAM17 and HOXA5. Dual luciferase reporter assays showed that miR-224 can directly regulate the expression of ADAM17 and HOXA5. Importantly, we found that miR-224 positively regulates cell migration and invasion in HCC, miR-224 overexpression can promote the migration and invasion of BEL-7402 cell, and miR-224 silencing can suppress the migration and invasion of BEL-7402 cell. miR-224 overexpression can result in the redistribution of cell cycle, the cell percentage of S phase was increased significantly, the cell percentage of G1 phase was decreased significantly, and there is no noticeable change for the cell percentage of G2 phase. These results demonstrated that it may be exert the function of oncogenes in a particular link of cancer cell growth. In conclusion, these results suggest that miR-224 will become a promising biological target in the treatment strategy of hepatocellular carcinoma (HCC).