C-terminal tensin-like (CTEN): a promising biomarker and target for cancer.

Int J Biochem Cell Biol

Department of Biochemistry and Molecular Medicine, University of California-Davis, Sacramento, CA 95817, United States. Electronic address:

Published: June 2014

AI Article Synopsis

  • C-terminal tensin-like (cten) is part of the tensin family, localized mainly at focal adhesion sites and has unique features in its structure.
  • Cten is highly expressed in healthy prostate and placenta tissues but is reduced in prostate cancer; however, its overexpression is linked to several cancer types, including breast and lung cancers.
  • Increased levels of cten enhance cell movement and tumor growth, suggesting it could be an important biomarker and target for cancer treatment.

Article Abstract

C-terminal tensin-like (cten, also known as tensin4, TNS4) is a member of the tensin family. Cten protein, like the other three tensin family members, localizes to focal adhesion sites but only shares sequence homology with other tensins at its C-terminal region, which contains the SH2 and PTB domains. Cten is abundantly expressed in normal prostate and placenta and is down-regulated in prostate cancer. However, overexpression of cten frequently associates with tumors derived from breast, colon, lung, stomach, skin and pancreas. A variety of cancer-associated growth factors and cytokines induce cten expression. Up-regulated cten promotes cell motility, prolongs epidermal growth factor receptor signaling, and enhances tumorigenicity. Emerging findings suggest that cten is a promising biomarker and therapeutic target for various cancers.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038153PMC
http://dx.doi.org/10.1016/j.biocel.2014.04.003DOI Listing

Publication Analysis

Top Keywords

c-terminal tensin-like
8
cten
8
tensin-like cten
8
cten promising
8
promising biomarker
8
tensin family
8
biomarker target
4
target cancer
4
cancer c-terminal
4
cten tensin4
4

Similar Publications

CTEN-induced TGF-β1 expression facilitates EMT and enhances paclitaxel resistance in bladder cancer cells.

Am J Transl Res

July 2024

Department of Urology Surgery, Hui Ya Hospital of The First Affiliated Hospital, Sun Yat-sen University Huizhou 516200, Guangdong, China.

Objectives: To investigate the role of C-terminal tensin-like (CTEN) in mediating chemotherapy resistance via epithelial-mesenchymal transition (EMT) in bladder cancer (BC) cells, through the regulation of transforming growth factor-β1 (TGF-β1) expression.

Methods: Lentiviral vectors were used to create CTEN overexpression and knockdown constructs, which were then introduced into paclitaxel-resistant BC cell lines. The effects of CTEN manipulation on cell proliferation and drug sensitivity was assessed using the CCK-8 assay, and apoptosis was evaluated by flow cytometry.

View Article and Find Full Text PDF

C-terminal tensin-like (tensin-4/TNS4/CTEN) is the fourth member of the tensin family, frequently described as displaying oncological functions, including cellular migration, invasion, adhesion, growth, metastasis, epithelial to mesenchymal transition, and apoptosis, in several different types of cancer. To investigate, for the first time, the clinical significance of CTEN in squamous cell carcinoma (SCC) of dogs, we studied a total of 45 SCC sections from various dog breeds. The mean age of the affected dogs was 8.

View Article and Find Full Text PDF

C-terminal tensin-like (CTEN) is a tensin family protein typically localized to the cytoplasmic side of focal adhesions, and primarily contributes to cell adhesion and migration. Elevated expression and nuclear accumulation of CTEN have been reported in several types of cancers and found to be associated with malignant behaviors. However, the function of nuclear CTEN remains elusive.

View Article and Find Full Text PDF

C-terminal tensin-like (CTEN) belongs to the tensin gene family, which encodes proteins that localize to focal adhesions and modulate integrin function. Accumulating studies have reported that CTEN expression can be upregulated or downregulated in different types of cancers, suggesting that CTEN has both oncogenic and tumor suppressor functions. In this study, by analyzing the expression level of CTEN in the human breast cancer (BRCA) samples from the clinically annotated genomic database, The Cancer Genome Atlas, we found that CTEN was downregulated in different BRCA subclasses, including luminal, human epidermal growth factor receptor 2 positive and triple-negative BRCA.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!