29119

CTNNA3

catenin (cadherin-associated protein), alpha 3;CTNNA3;catenin (cadherin-associated protein), alpha 3

alpha-T-catenin|alpha-catenin-like protein|catenin alpha-3

10q22.2

protein-coding

Human microRNA-9 (miR-9) has been reported to be involved in the metastasis of several malignancies including brain breast cancer. However, its role in the metastasis of colorectal cancer (CRC) remains to be revealed. Here, we evaluated miR-9 expression in metastatic CRC and investigated its effects on the motility and proliferation of RKO cells. The expressions of miR-9 in 15 primary CRC specimens without distant metastasis (NM group) and 10 primary CRC specimens (M group) with distant metastasis (M group) were determined by quantitative real-time PCR. The alternations in the motility and morphology of RKO cells before and after miR-9 transfection were analyzed by migration assay and F-actin staining. The relationship between miR-9 and alpha-catenin was identified by Western blotting. Cell growth was examined by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazoliumbromide) assay. Significant difference of miR-9 expression was observed in M group compared to the NM group (P < 0.001). Ectopic expression of miR-9 enhanced the motility of RKO cells as well as changed their morphological appearance, while cell growth remained unchanged. The overexpression of miR-9 could also down-regulate alpha-catenin expression. These data suggest that miR-9 may potentially participate in the metastatic process of CRC though facilitating cell motility.

BACKGROUND: Currently available methods for diagnosis and staging of prostate cancer lack the sensitivity to distinguish between patients with indolent prostate cancer and those requiring radical treatment. Alterations in key adherens (AJ) and tight junction (TJ) components have been hailed as potential biomarkers for prostate cancer progression but the majority of research has been carried out on individual molecules. OBJECTIVE: To elucidate a panel of biomarkers that may help distinguish dormant prostate cancer from aggressive metastatic disease. METHODS: We analysed the expression of 7 well known AJ and TJ components in cell lines derived from normal prostate epithelial tissue (PNT2), non-invasive (CAHPV-10) and invasive prostate cancer (LNCaP, DU145, PC-3) using gene expression, western blotting and immunofluorescence techniques. RESULTS: Claudin 7, alpha -catenin and beta-catenin protein expression were not significantly different between CAHPV-10 cells and PNT2 cells. However, in PC-3 cells, protein levels for claudin 7, alpha -catenin were significantly down regulated (-1.5 fold, p = <.001) or undetectable respectively. Immunofluoresence showed beta-catenin localisation in PC-3 cells to be cytoplasmic as opposed to membraneous. CONCLUSION: These results suggest aberrant Claudin 7, alpha - and beta-catenin expression and/or localisation patterns may be putative markers for distinguishing localised prostate cancer from aggressive metastatic disease when used collectively.