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Collagen triple helix repeat containing 1 promotes endometrial cancer cell migration by activating the focal adhesion kinase signaling pathway

Metastasis of endometrial cancer (EC) is known to be the major cause of relapse and death of patients. However, the mechanisms of this process are not well understood. Focal adhesion kinase (FAK) is known for its essential role in integrin signaling and is highly expressed in many human tumors. FAK...

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Detalles Bibliográficos
Autores principales: Hu, Xiang, Bian, Yiding, Wen, Xiaoli, Wang, Mengfei, Li, Yiran, Wan, Xiaoping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388291/
https://www.ncbi.nlm.nih.gov/pubmed/32742375
http://dx.doi.org/10.3892/etm.2020.8833
Descripción
Sumario:Metastasis of endometrial cancer (EC) is known to be the major cause of relapse and death of patients. However, the mechanisms of this process are not well understood. Focal adhesion kinase (FAK) is known for its essential role in integrin signaling and is highly expressed in many human tumors. FAK also plays important roles in a variety of cellular processes. Collagen triple helix repeat containing 1 (CTHRC1) is a secreted protein that has been detected in many human solid cancers. In the present study, CTHRC1 was found to be highly expressed in EC tissues when compared with normal tissues. In addition, overexpression of CTHRC1 promoted the migration of EC cells in vitro. Recombinant CTHRC1 protein also promoted the migration of EC cells in vitro. The results of the present study suggested that CTHRC1 mediated EC cell migration via the FAK signaling pathway. Taken together, these data indicated that CTHRC1 and the FAK signaling pathway may be potential therapeutic targets for EC metastasis treatment.