Cortactin promotes colorectal cancer cell proliferation by activating the EGFR-MAPK pathway.
Cortactin promotes colorectal cancer cell proliferation by activating the EGFR-MAPK pathway.
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Cortactin 通过激活 EGFR-MAPK 通路促进结直肠癌细胞增殖
DOI：
10.18632/oncotarget.13652
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发表时间：
2017-01-03
期刊：
影响因子：
--
通讯作者：
Zhao R
中科院分区：
文献类型：
--
作者：
Zhang X;Liu K;Zhang T;Wang Z;Qin X;Jing X;Wu H;Ji X;He Y;Zhao R
皮质蛋白（CTTN）在包括头颈部鳞状细胞癌和结直肠癌（CRC）在内的多种肿瘤中过表达，可作为肿瘤转移的生物标志物。我们观察到CTTN在体外促进癌细胞增殖，并在体内增加CRC肿瘤异种移植物的生长。CTTN表达增加EGFR蛋白水平，增强MAPK信号通路的激活。CTTN的表达也通过抑制c-Cbl与EGFR的偶联来抑制泛素介导的EGFR降解。CoIP实验表明，CTTN可与CRC细胞中的c-Cbl相互作用。这些结果表明，CTTN促进CRC细胞的增殖，抑制EGFR的降解。
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.