Abstract
Asporin has been implicated as an oncogene in various types of human cancers; however, the roles of asporin in the development and progression of colorectal cancer (CRC) have not yet been determined. With clinical samples, we found that asporin was highly expressed in CRC tissues compared to adjacent normal tissues and the asporin expression levels were significantly associated with lymph node metastasis status and TNM stage of the patients. Through knockdown of asporin in CRC cell lines RKO and SW620 or overexpression of asporin in cell lines HT-29 and LoVo, we found that asporin could enhance wound healing, migration and invasion abilities of the CRC cells. Further more, with the human umbilical vein endothelial cells (HUVECs) tube formation assays and the xenograft model, we found that asporin promoted the tumor growth through stimulating the VEGF signaling pathway. The portal vein injection models suggested that asporin overexpression stimulated the liver metastasis of HT29 cell line, while asporin knockdown inhibited the liver metastasis of RKO cell line. In addition, asporin was found to augment the phosphorylation of EGFR/Src/cortactin signaling pathway, which might be contributed to the biological functions of asporin in CRC metastasis. These results suggested that asporin promoted the tumor growth and metastasis of CRC, and it could be a potential therapeutic target for CRC patients in future.
Highlights
Colorectal cancer (CRC) is one of the most common causes of cancer-related death worldwide [1]
We found that asporin was highly expressed in colorectal cancer (CRC) tissues compared to adjacent normal tissues and the asporin expression levels were significantly associated with lymph node metastasis status and TNM stage of the patients
With the human umbilical vein endothelial cells (HUVECs) tube formation assays and the xenograft model, we found that asporin promoted the tumor growth through stimulating the VEGF signaling pathway
Summary
Colorectal cancer (CRC) is one of the most common causes of cancer-related death worldwide [1]. Patients with metastatic CRC have a 5-year survival rate of only 11.7% [3]. Elucidating the molecular mechanisms involved in the initiation and progression of CRC may provide biomarkers for early detection and targeted therapy. Known as periodontal ligamentassociated protein (PLAP1), is an extracellular matrix (ECM) protein. It belongs to the small leucinerich proteoglycans (SLRPs) family and contains a unique aspartate-rich N terminus that distinguishes it from other SLRPs family members [4]. Whether asporin is involved in the CRC development and progression has not been clarified. For the first time, we evaluated the clinical relevance of the asporin expression in CRC and determined the underlying mechanisms for the oncogenic activities of asporin in the CRC development and progression
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