University of Nevada, Reno
Appointment period: 2/1/2015 to 11/30/2015
Cten in tumorigenesis
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. Unlike other tensin members, cten also translocates to nuclei. 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. Up-regulated cten promotes cell motility, prolongs epidermal growth factor receptor (EGFR) signaling, and enhances tumorigenicity. Emerging findings suggest that cten is a promising biomarker and therapeutic target for various cancers.
My research focuses on investigating cten’s roles in cancer development and the potential of targeting cten together with EGFR in treating cancer, using biochemistry and molecular/cellular biology approaches, as well as, cten mouse models.