Crk-like adapter protein is overexpressed in cervical carcinoma, facilitates proliferation, invasion and chemoresistance, and regulates Src and Akt signaling.

Abstract

Overexpression of Crk-like (CrkL) adapter protein has been implicated in a number of types of human cancer. However, its involvement in human cervical carcinoma remains unclear. The present study aimed to explore the clinical significance and biological characteristics of CrkL in human cervical carcinoma. CrkL protein expression was examined in tissue samples from 92 cases of cervical carcinoma using immunohistochemistry, and was found to be overexpressed in 48.9% (45/92 cases). CrkL was transfected into HeLa and CaSki cervical carcinoma cell lines and its effects on biological behavior were examined. CrkL overexpression was revealed to promote cell proliferation, invasion and chemoresistance. In addition, CrkL overexpression increased the level of Src and Akt phosphorylation. Treatment with the Src inhibitor dasatinib eliminated the effect of CrkL on cell invasion. In conclusion, the current results demonstrate that CrkL is an oncoprotein overexpressed in cervical carcinoma which contributes to malignant cell growth and chemoresistance. In addition, the findings indicate that CrkL promotes cervical cancer cell invasion through a Src-dependent pathway.