Abstract
The chemokine CXCL10 and its receptor CXCR3 have been demonstrated to be implicated in cancer cell proliferation and metastasis. CXCR3 has three splice variants: CXCR3A, CXCR3B and CXCR3-alt. CXCR3A and B serve multiple roles in the growth and invasiveness of a number of cancer types. However, the roles of CXCR3 isoforms in colorectal cancer (CRC) cells remain unclear. In the current study, the effects of CXCL10 and CXCR3 isoforms on proliferation and invasion of CRC cells was examined. Proliferation and invasiveness of the CRC cell line HCT116, which were transfected with CXCR3A or CXCR3B in the presence of CXCL10, were evaluated in vitro using MTT, scratch wound healing and transwell assays. MTT assay indicated that regardless of the presence or absence of CXCL10, the proliferative ability of CXCR3A-transfected HCT116 cells was enhanced compared with blank and mock cells. Scratch wound healing and transwell assays indicated that invasiveness of CXCR3A-transfected cells was greater compared with blank and mock cells. However, HCT116 cells transfected with CXCR3B did not exhibit changes in their proliferative or invasive ability. mRNA expression of MMP9, which is associated with signaling downstream of the CXCL10/CXCR3A pathway, was increased 4-fold in CXCR3A-transfected HCT116 cells compared with control cells. The results of the present study indicated that CXCL10-enhanced proliferation and invasiveness of the CRC cell line HCT116 was likely mediated by CXCR3A, but not by CXCR3B.