Research Papers:
Cortactin promotes colorectal cancer cell proliferation by activating the EGFR-MAPK pathway
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Abstract
Xiaojian Zhang1,2,*, Kun Liu3,*, Tao Zhang1, Zhenlei Wang1,4, Xuan Qin1,2, Xiaoqian Jing1,2, Haoxuan Wu1,2, Xiaopin Ji1, Yonggang He1, Ren Zhao1
1Department of Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
2Shanghai Institute of Digestive Surgery, Shanghai, People’s Republic of China
3Department of Surgery, Ruijin Hospital North, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
4Department of Surgery, Henan Cancer Hospital, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, Henan Province, People’s Republic of China
*These authors have contributed equally to this work
Correspondence to:
Ren Zhao, email: [email protected]
Keywords: colorectal cancer, cortactin(CTTN), epidermal growth factor receptor (EGFR), MAPK, c-Cbl
Received: August 16, 2016 Accepted: November 15, 2016 Published: November 26, 2016
ABSTRACT
Cortactin (CTTN) is overexpressed in various tumors, including head and neck squamous cell carcinoma and colorectal cancer (CRC), and can serve as a biomarker of cancer metastasis. We observed that CTTN promotes cancer cell proliferation in vitro and increases CRC tumor xenograft growth in vivo. CTTN expression increases EGFR protein levels and enhances the activation of the MAPK signaling pathway. CTTN expression also inhibits the ubiquitin-mediated degradation of EGFR by suppressing the coupling of c-Cbl with EGFR. CoIP experiments indicate CTTN can interact with c-Cbl in CRC cells. These results demonstrate that CTTN promotes the proliferation of CRC cells and suppresses the degradation of EGFR.
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