| Gene information | Literature | Expression | lncRNA | Mutation | Homolog |
Basic Information | |
|---|---|
Gene ID | 84951 |
Name | TNS4 |
Synonymous | tensin 4;TNS4;tensin 4 |
Definition | C terminal tensin like|C-terminal tensin-like protein|tensin-4 |
Position | 17q21.2 |
Gene type | protein-coding |
Title | Abstract |
| CTEN (C-terminal tensin-like), a novel oncogene overexpressed in invasive breast carcinoma of poor prognosis. | C-terminal tensin-like (CTEN) gene is a member of the TENSIN gene family, involved in cell migration and localised at focal adhesion sites. This study was designed to explore the prevalence and clinical significance of CTEN expression in a large and well-characterised series (n = 1,409) invasive breast cancer (BC) cases with long term follow-up (median 11 years), using immuno-histochemistry and tissue microarray. Moderate to strong cytoplasmic immunoreactivity for CTEN was observed in 90% of the studied cases. CTEN expression was significantly associated with poor prognostic variables including larger tumour size (P = 0.044), higher histological grade (P = 0.019), axillary nodal involvement (P = 0.035) and poor Nottingham Prognostic Index (P = 0.016). Significant associations were observed between increased CTEN expression and up-regulation of phosphorylated-Akt (P-Akt), PIK3 and N-cadherin proteins (P .001). Kaplan-Meier survival analysis demonstrated that patients with high CTEN expression had significantly shorter Breast cancer Specific Survival (P = 0.004) and Metastasis-Free Survival (P = 0.041) than those with low-CTEN expression. Multivariate analysis showed that CTEN was not an independent prognostic marker in BC. In conclusion, our results demonstrated the oncogenetic role of increased CTEN expression and its association with poor prognostic parameters. These data could help in prognostic assessment in BC patients. |
| C-terminal tensin-like gene functions as an oncogene and promotes cell motility in pancreatic cancer. | OBJECTIVES: C-terminal tensin-like gene (CTEN, also known as TNS4) localizes to focal adhesions and is reported to function as an oncogene in colonic, breast, lung, and gastric cancers. Its role in pancreatic cancer is unknown and was thus investigated in this study. METHODS: C-terminal tensinlike gene expression was evaluated by immunohistochemistry in a series of pancreatic cancers. Functional activity of the CTEN was tested by manipulating cellular CTEN levels using a dual approach of gene knockdown/forced expression. RESULTS: The CTEN is overexpressed in 31 (70.45%) of 44 pancreatic cancers. Functionally, changes in CTEN level did not alter cellular proliferation, but CTEN levels were positively associated with enhanced colony-forming efficiency in both Panc-1 and PSN-1 cell lines. Forced CTEN expression in Panc-1 cells stimulated cell motility, whereas knockdown of CTEN in PSN-1 inhibited cell motility in both transwell migration and wound-healing assays. Evaluation of downstream targets demonstrated that alterations in CTEN levels induced changes in focal adhesion kinase and E-cadherin, whereas integrin-linked kinase (ILK) remained unchanged. CONCLUSIONS: These are the first data showing an oncogenic role for CTEN in pancreatic cancer through promotion of colony formation and cell motility. The latter may be mediated by signaling through focal adhesion kinase and inhibiting E-cadherin. |