To investigate the astrocyte elevated gene-1 (AEG-1) expression and its relationship with the clinicopathological features of colorectal carcinoma (CRC) and β-catenin signaling pathway. Real-time PCR, Western blot, immunohistochemistry, and immunofluorescence staining were performed to detect AEG-1 expression in CRC cell lines, 8 pairs of fresh CRC and adjacent nontumor tissues (ANT), 120 pairs of paraffin-embedded CRC specimens and ANT tissues, and 60 samples of lymph node metastatic CRC tissues. Scratch wound assay and transwell matrix penetration assay were performed to determine migration and invasion of SW480 cell lines with stable AEG-1 overexpression or SW620 cell lines with AEG-1 knockdown. AEG-1 expression was upregulated in CRC cell lines and tissues compared with ANT. Furthermore, AEG-1 expression level significantly correlated with UICC stage, and the N classification. AEG-1 overexpression significantly enhanced migration and invasion of SW480 cell lines. However, AEG-1 knockdown suppressed migration and invasion of SW620 cell lines. Meanwhile, there was a positive correlation between AEG-1 high expression and β-catenin nuclear expression in CRC. AEG-1 overexpression increased nuclear β-catenin accumulation in CRC cell lines. AEG-1 knockdown decreased nuclear β-catenin accumulation in CRC cell lines. Moreover, we firstly found that AEG-1 interacted with β-catenin in SW480 cell lines. Our results for the first time showed that AEG-1 interacted with β-catenin in CRC cells and AEG-1 expression was closely associated with progression of CRC. AEG-1 might be a potential therapeutic target in CRC.

This paper aimed to study whether Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) regulates β-catenin signaling pathway in nasopharyngeal carcinoma (NPC). Western blotting, immunofluorescence, luciferase reporter assay, co-immunoprecipitation assay, and immunohistochemistry staining were used. LMP1 increased β-catenin transcriptional activity in NPC cell lines. The upregulation of β-catenin transcriptional activity induced by LMP1 was much higher in poorly differentiated NPC cell line CNE2 than that in well-differentiated NPC cell line CNE1. Immunofluorescence staining and Western blotting also showed that LMP1 increased nuclear β-catenin accumulation in NPC cell lines. Moreover, LMP1 expression was closely related to abnormal β-catenin expression in NPC tissues by immunohistochemistry. LMP1 may be involved in nasopharyngeal carcinogenesis via β-catenin signaling pathway.