AURKB promotes tumorigenesis and carboplatin resistance by regulating the ERK pathway in neuroblastoma cells.

BACKGROUND: Previous research has revealed that activation or aberrant expression of kinases can lead to tumorigenesis of various cancers, including neuroblastoma (NB). Suppression of kinase expression can reduce drug resistance. We explored the potential role and mechanism of the aurora kinase B (AURKB) gene in the acquisition of carboplatin resistance in NB. METHODS: Immunohistochemistry (IHC) and qRT-PCR were used to explore the AURKB expression in NB patients. Subsequently, we structured Carboplatin-resistant NB cells. The potential biological functions of AURKB in carboplatin resistance were examined through knockdown of AURKB combined with CCK8, flow cytometry, immunohistochemistry, and western blot. Finally, overexpression of AURKB combined with ERK inhibitor (U0126) was carried out to explore the role of downstream signaling pathways. RESULTS: Overexpression of AURKB was closely correlated to poor prognosis in NB patients. In vitro, knockdown of AURKB could lead to a decline in IC50 value and restrain the invasion and the expression of MRP1 and Ki67, while promotes apoptosis in carboplatin-resistant cells (IMR-32-R and SK-N-AS-R). Additionally, AURKB overexpression could potentiate the invasion and the expression of MRP1 and Ki67, while suppresses apoptosis in SK-N-AS-R and IMR-32-R, whereas ERK inhibitor U0126 could reverse the phenomenon caused by AURKB overexpression. CONCLUSION: AURKB overexpression was strongly associated with poor prognosis and carboplatin resistant acquisition. Additionally, suppression of AURKB-ERK axis might be a potential therapy for carboplatin resistance in NB patients.

Clinical value of color Doppler ultrasound combined with serum tumor markers for the diagnosis of medullary thyroid carcinoma.

The present study aimed to explore the clinical value of color Doppler ultrasound combined with serum tumor markers, including calcitonin (CT) and carcinoembryonic antigen (CEA), for the diagnosis of medullary thyroid carcinoma (MTC). A total of 39 patients with MTC (MTC group), 50 patients with papillary thyroid carcinoma (PTC) (PTC group) and 30 patients with thyroid adenoma (benign control group) were enrolled in the present study. The patients were hospitalized at the Affiliated Hospital of Qingdao University from January 2012 to December 2018 and were diagnosed through surgical procedures and pathology laboratory results. The ultrasound results, as well as serum CT and CEA results, were collected and analyzed. A significant difference was observed between the MTC and PTC groups in regards to morphology, margin, aspect ratio, calcification, internal blood flow and lymph node metastasis (all P<0.01). There was also a significant difference between the MTC and benign control group in regards to internal echo, calcification, internal blood flow and lymph node metastasis (all P<0.01). In addition, the levels of serum CT and CEA in the MTC group were significantly higher than those in the PTC and the benign control groups (both P<0.01). For patients with MTC, the levels of serum CT and CEA were significantly associated with maximum tumor diameter, lymph node metastasis and the patient state after treatment (all P<0.01). Furthermore, the sensitivities of ultrasound, serum CT and CEA for the diagnosis of MTC were 76.92, 74.36 and 68.23%, respectively. The value for the combination of the three markers (94.87%) was significantly higher compared with the sensitivity value of each separate marker (all P<0.05). In conclusion, color Doppler ultrasound combined with detecting the levels of serum tumor markers (CT and CEA) significantly improved the diagnostic efficiency for MTC, which could be useful for the clinical diagnosis and treatment of MTC.

MicroRNA-758 acts as a tumor inhibitor in colorectal cancer through targeting PAX6 and regulating PI3K/AKT pathway.

Recently, a number of microRNAs (miRNAs) have been reported to play different roles in human cancers, including colorectal cancer (CRC). However, the specific role of miR-758 has not been clarified in CRC. Therefore, the aim of the present study was to explore the role of miR-758 in CRC. RT-qPCR and western blot analysis were used to quantify the expression of miR-758 and genes. The function of miR-758 in CRC was investigated using Transwell, CCK-8 and luciferase reporter assays. According to the results, the downregulation of miR-758 expression was associated with aggressive behavior and poor prognosis in CRC patients. miR-758 was shown to restrain the cell viability and metastasis in CRC. In addition, it was confirmed that miR-758 directly targets PAX6 and inhibits CRC progression through targeting PAX6. The results also revealed that miR-758 blocked EMT and PI3K/AKT pathway in CRC. In conclusion, miR-758 acts as a tumor suppressor in CRC by downregulating PAX6.