Cataracts are the most common eye disease to cause blindness in patients. The abnormal deposition of laminins (LMs) in the lens capsule and the disruption of capsular epithelium contribute to cataract development, although the mechanism by which this occurs is currently unclear. The present study aimed to reproduce HLE B-3 basement membranes (BMs) using HLE B-3 cells and to analyze the similarities of LM expression between HLE B-3 BMs and human anterior lens capsule (ALC). Immunohistochemistry (IHC), ELISA, western blot analysis and immunoprecipitation (IP)-western blot analysis were used to detect total LMs, LM trimers and 11 LM subunits in HLE B-3 cells, HLE B-3 BMs and human ALCs. In IHC staining, HLE B-3 cells and human ALCs were positive for LMs. In LM ELISA, all samples analyzed were positive for LMs. Western blot analysis detected all LM subunits except for LMγ3 in HLE B-3 cell lysate, 4 subunits (LMα4, LMα2, LMα1 and LMγ1) in HLE B-3 cell culture supernatant, 5 subunits (LMα4, LMα2, LMα1, LMβ3 and LMγ1) in HLE B-3 BMs, and 3 subunits (LMα4, LMγ2 and LMγ1) in human ALCs. The results of IP-western blot analysis revealed that the LM411 trimer was detected in HLE B-3 cell culture supernatant. These results indicated that HLE B-3 BMs were similar to human ALCs in terms of LM expression. Therefore, HLE B-3 BMs could be used as an in vitro ALC model to determine the role of LMs in ALC in the pathogenesis of cataracts and to select potential anti-cataract drugs.

Oral squamous cell carcinoma (OSCC) is a common human malignancy with a high incidence rate and poor prognosis. Although astrocyte elevated gene 1 (AEG-1) expression is up-regulated in various human cancers and plays an important role in carcinogenesis and tumour progression, the impact of AEG-1 on the development and progression of OSCC remains unclear. Accordingly, this study aims to clarify the biological significance of AEG-1 in OSCC. We found AEG-1 to be overexpressed in OSCC tissues compared to normal oral mucosa. Knockdown or overexpression of AEG-1 in OSCC cell lines showed that AEG-1 is important for tumour growth, apoptosis, drug tolerance, and maintaining epithelial-mesenchymal transition (EMT)-mediated cell migration and invasion in vitro. Moreover, in a xenograft-mouse model generated by AEG-1-overexpressing SCC15 cells, we found that higher expression of AEG-1 promoted tumour growth, angiogenesis, and EMT in vivo. These findings provide mechanistic insight into the role of AEG-1 in regulating OSCC tumour growth, apoptosis, drug tolerance, and invasion, as well as AEG-1-induced activation of p38 and NF-κB signalling, suggesting that AEG-1 is an important prognostic factor and therapeutic target for OSCC.Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. Each year, 1.6 million new cases of HNSCC are diagnosed, with half localized in the oral cavity (oral squamous cell carcinoma, OSCC), and 33,3000 deaths 1 . Indeed, OSCC is an important component of the worldwide cancer burden; despite radical surgery combined with radiation, chemotherapy and targeted therapy, OSCC has a 5-year survival rate of only approximately 50% 2 . The pathogenesis of OSCC is complex, involving many genes and pathways, though the mechanism of OSCC development remains unclear.Metastasis is dependent on unique mechanisms by which cancer cells escape from the primary tissue and spread to surrounding tissues. As part of the epithelial-mesenchymal transition (EMT), molecular reprogramming is a crucial step in the metastasis of most carcinomas 3 . During metastatic progression, EMT causes primary epithelial-like tumour cells to acquire invasive potential, including increased motility and mesenchymal characteristics, which results in dissemination from the original tumour and intravasation into the tumour vessel. EMT-driven cells circulating in the blood then redifferentiate into a primary status via the mesenchymal-epithelial transition (MET) during colonisation of and growth at distant metastatic sites 4,5 . Because of the important roles of EMT in the metastatic process, controlling EMT progression in tumours is thought to be a promising strategy to inhibit metastasis and prolong patient survival.Astrocyte elevated gene-1 (AEG-1), also known as metadherin (MTDH) or LYsine-RIch CEACAM1 co-isolated (LYRIC), is a 582-amino acid, type II transmembrane protein without any known functional domains. Recently, numerous reports have demonstrated that AEG-1 might play a pivotal role in the pathogenesis, ...

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Prolonged glucocorticoids (GCs) treatment may lead to the formation of posterior subcapsular cataracts. The present study aimed to investigate differential gene expression in lens epithelial cells (LECs) in response to GCs using DNA microarray profiling. The gene expression profile of GSE13040 was downloaded from the Gene Expression Omnibus database, which includes 12 human LECs treated with vehicle or dexamethasone (Dex) for 4 or 16 h with six samples at each time period, of which three samples were treated with vehicle (control group) and three samples were treated with Dex (Dex group) at each time point. The differentially expressed genes (DEGs) were identified between the control group and the Dex group at each time period with the thresholds of P<0.05 and |logFC|>1. The DEGs were further analyzed using bioinformatics methods. Firstly, DEGs were subject to a hierarchical cluster analysis. Subsequently, the functional enrichment analysis was performed for the common DEGs between the two time periods. Finally, the transcription factors and binding sites of DEGs associated with response to GC stimulus were analyzed. A total of 696 and 949 DEGs were identified at 4 h and 16 h, respectively. Hierarchical cluster analysis revealed that DEG expression was higher in the Dex group than in the control group (P<0.05). A total of 13 significant functions were enriched for the 72 common DEGs at the two time periods. Chemokine (C-C motif) ligand 2 (CCL2), dual-specificity phosphatase-1 (DUSP1) and FAS were associated with the response to GC stimulus and the transcription factor c-Jun bound to promoter regulation regions of CCL2, DUSP1 and FAS. In conclusion, the transcription factors and binding sites of DEGs associated with the response of LECs to GCs may provide potential gene targets for designing and developing drugs to protect against GC-induced cataract formation.