UBE2C affects breast cancer proliferation through the AKT/mTOR signaling pathway.

BACKGROUND: Ubiquitin-conjugating enzyme E2C (UBE2C) has been shown to be associated with the occurrence of various cancers and involved in many tumorigenic processes. This study aimed to investigate the specific molecular mechanism through which UBE2C affects breast cancer (BC) proliferation. METHODS: BC-related datasets were screened according to filter criteria in the Gene Expression Omnibus (GEO) database and The Cancer Genome Atlas (TCGA) database. Then differentially expressed genes (DEGs) were identified using Venn diagram analysis. By using DEGs, we conducted the following analyses including Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), protein-protein interaction (PPI), and survival analysis, and then validated the function of the hub gene UBE2C using quantitative reverse transcription-polymerase chain reaction (RT-qPCR), cell counting kit-8 (CCK-8) assay, transwell assay, and Western blot assay. RESULTS: In total, 151 DEGs were identified from the GEO and TCGA databases. The results of GO analysis demonstrated that the DEGs were significantly enriched with mitotic nuclear division, lipid droplet, and organic acid-binding. KEGG analysis showed that the peroxisome proliferators-activated receptor (PPAR) signaling pathway, regulation of lipolysis in adipocytes, and proximal tubule bicarbonate reclamation were significantly enriched in the signal transduction pathway category. The top three hub genes that resulted from the PPI network were FOXM1, UBE2C, and CDKN3. The results of survival analysis showed a close relationship between UBE2C and BC. The results of CCK-8 and transwell assays suggested that the proliferation and invasion of UBE2C knockdown cells were significantly inhibited (P < 0.050). The results of Western blot assay showed that the level of phosphorylated phosphatase and tensin homology deleted on chromosome 10 (p-PTEN) was obviously increased (P < 0.050), whereas the levels of phosphorylated protein kinase B (p-AKT), phosphorylated mammalian target of rapamycin (p-mTOR), and hypoxia-inducible factor-1 alpha (HIF-1α) were dramatically decreased (P < 0.050) in the UBE2C knockdown cell. CONCLUSION: UBE2C can promote BC proliferation by activating the AKT/mTOR signaling pathway.

[Characteristics of Ozone Background Concentration in Beijing from 2004 to 2015].

Based on the hourly O3 monitoring data from 2004 to 2015 of Beijing, a comprehensive discussion on the characteristics of O3 concentration at a background station Dingling in Beijing was conducted. The results showed that the annual concentration of O31h was increasing with a growth rate of 4.40 µg·m-3 while the annual concentration of O38h was decreasing with annual average rates of -1.0 µg·m-3 and -1.5 µg·m-3 from May to October in 2004 and 2015. Over the past 3 years, number of O38h severe pollution days increased significantly and the situation of O3 pollution in Beijing became more serious. O3 concentration reached its peak in June in a year and its diurnal peak concentration occurred at about 15:00-18:00 at Dingling station which was 101-1.56 times larger than that in the urban center of Beijing. In different years, the ozone peak concentration at Dingling Station was 1h later than that in the urban center from May to October in diurnal variation and the difference of peak concentration was significantly reduced in recent years, which on the one hand may be related to regional ozone pollution, on the other hand may be related to the expansion of Beijing's urbanization.