CXCL2 participates in NDRG3-mediated colorectal cancer metastasis

Abstract

Abstract Purpose: In our previous work, we showed that NDRG3 facilitated colorectal cancer (CRC) metastasis, yet the molecular mechanism underlying NDRG3-mediated CRC metastasis has not been elucidated. Thus, we explored the role of chemokine (C-X-C motif) ligand 2 (CXCL2) in NDRG3-mediated CRC metastasis. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry were used to detected the expression of CXCL2 in CRC. CXCL2 was modified in RKO/shNDRG3 and SW1116/NDRG3 cells. Wound healing assay, invasion assay and xenograft model were then introduced to determine the role of CXCL2 in NDRG3-mediated CRC metastasis. Western blotting analysis was used to investigate the potential mechanism of CXCL2 in CRC metastasis. Results: CXCL2 was highly expressed in CRC tissue. CXCL2 contributed to the invasion of CRC cells, and acted as a downstream target of NDRG3. Knockdown of CXCL2 abolished the NDRG3-mediated invasive capacity of SW1116 cells, whereas the overexpression of CXCL2 enhanced the invasiveness of the RKO/shNDRG3 cells. Similar results were obtained in the xenograft model. Western blot result showed that CXCL2 knockdown inhibits Src activation in SW1116/NDRG3 cells. Conclusion: CXCL2 serves as an oncogene in CRC and participates in NDRG3-mediated CRC metastasis.