To study the oncogenic role of Rhotekin, a RhoGTPase effector
Date Issued
2008
Date
2008
Author(s)
Peng, Wen-Hsin
Abstract
Gastric cancer is ranked the fourth common cancer and the second leading cause ofancer death worldwide (almost 1 million deaths/year).Using ordered differentialisplay, we have identified rhotekin, the gene encoding Rho effector rhotekin (RTKN)s one of the genes overexpressed in human gastric cancer. To further understand theole of Rho/RTKN involved in the pathogenic development of GC, in this study, weropose to dissect Rho signaling pathways that are mediated by RTKN, and specialfforts will be focused on the ones contribute to malignant transformation and tumoretastasis. To assess the function of RTKN in cellular transformation, we ectopicallyxpressed RTKN in cultured cell, and monitored the biological readouts of RTKNxpression. The data shown, RTKN expression suppressed contact inhibition ofovement in both H1299 as well as HEK293 cells. RTKN In consistence,verexpression of RTKN conferred an increased saturation density in H1299 cells.verexpression induced extensive cell surface protrusions with a concomitant decreasef stress fibers and focal adhesions. We have further generated stable clones : H1299nd AZ-521, RTKN low expresser that stably expressed RTKN, and NUGC-3 , RTKNigh expresser that stably knock downed RTKN, and tested for transforming activity.he stable clone displayed increased migration and invasion ability when compared tohe parental cells. In addition, the stable clone developed anchorage-independent growthn soft agar whereas the parental cells showed reduced growth in soft agar. Takenogether, we conclude that overexpression of RTKN may promote cell transformationnd cell migration, and thus and thus contribute to tumor metastasis.
Subjects
Cancer
Cell transformation
Cell migration
Cell invasion
Anchorage-independent growth
SDGs
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