RESUMO
Adipocyte enhancer binding protein 2, as a component protein of Polycomb repressive complex (PRC2), is involved in the proliferation and migration of many tumor cells. However, its role in HCC is still unclear. In this study, we identify that AEBP2 was upregulated in HCC samples from the UALCAN and Kaplan-Meier Plotter database, which was correlated to the overall survival time of HCC patients. Real-time quantitative PCR and Western blotting confirmed that the expression of AEBP2 in HCC cells was higher than normal liver cells. After silencing AEBP2 in HepG2 and Huh-7 cells, the effects of the proliferation, apoptosis, migration and invasion were detected by colony formation, CCK-8, flow cytometry, scratch healing and Transwell chamber, respectively. Compared with the control group, down-regulation of AEBP2 expression inhibited the proliferation, migration and invasion in HepG2 and Huh-7 cells, as well as promoted apoptosis (P<0. 05). Immunofluorescence and Western blotting results showed that AEBP2 silencing inhibited epithelial-mesenchymal transformation (EMT) (P < 0. 05). Bioinformatics analysis showed that AEBP2 is involved the PI3K/Akt signaling pathway. Western blotting results confirmed that silencing AEBP2 down-regulated the expression levels of PI3K, p-AKT (S473), mTOR, MMP-2 and MMP-9 proteins (P<0. 05). In addition, the effects of AEBP2 silencing on HepG2 cells migration and invasion could be reversed by PI3K/Akt pathway agonist insulin-like Growth Factors (IGF-1) (P < 0. 01). In summary, our study showed that AEBP2 promoted the proliferation and migration of HCC cell by regulating PI3K/AKT pathway. This study provided a theoretical basis for the role of AEBP2 in HCC.
RESUMO
OBJECTIVE@#To study the correlation of galectin-3 level in bronchoalveolar lavage fluid (BALF) with Mycoplasma pneumoniae (MP) load and cellular immunity of neutrophils and macrophages in the airway in children with refractory MP pneumonia (RMPP).@*METHODS@#A total of 64 children with RMPP who were hospitalized from January 2013 to January 2017 were enrolled. In addition to the conservative medical treatment, all the 64 children with RMPP were given bronchoalveolar lavage in the acute stage (5-7 days after admission) and 48 out of the 64 children were given bronchoalveolar lavage in the recovery stage (10-14 days after admission). Four milliliters of BALF of the affected lung lobe or segment were collected. ELISA was used to measure the level of galectin-3 in BALF supernatant. RT-PCR was used to measure MP load. Hematoxylin and eosin staining was used to measure the percentage of neutrophils and macrophages. Six children with bronchial foreign bodies were enrolled as the control group.@*RESULTS@#The RMPP group had a significantly higher level of galectin-3 in BALF in both the acute and recovery stages than the control group (P0.05). The RMPP group had a significantly higher MP load in BALF in both the acute and recovery stages than the control group (P<0.01), and the MP load in the acute stage was significantly higher than in the recovery stage (P<0.01). In the children with RMPP, galectin-3 level in BALF in the acute stage was positively correlated with MP load and the percentage of neutrophils (r=0.789 and 0.726 respectively; P<0.01).@*CONCLUSIONS@#Galectin-3 is involved in the process of airway inflammation in children with RMPP, and the level of galectin-3 in BALF is positively correlated with MP load. RMPP is a cellular immune inflammatory lesion with the increase of neutrophils and the reduction in macrophages. Galectin-3 is closely associated with neutrophil chemotaxis and luminal infiltration in children with RMPP. MP load gradually decreases with the recovery from RMPP, but it is not completely eliminated by the immune system in the recovery stage. MP infection can increase the consumption of macrophages in children with RMPP.