Objective To explore the expression of collagen triple helix repeat containing 1 (CTHRC1) in colorectal cancer and study its role in regulating the biological behaviors of colorectal cancer LoVo cells in vitro. Methods Real-time PCR and Western blotting were used to detect the expressions of CTHRC1 in colorectal cancer tissue and paired adjacent nontumorous tissue and in 5 colorectal cancer cells. pGPU6-CTHRC1-shRNA was transfected into LoVo cells and the changes in cell proliferation was assessed using cell counting kit-8 (CCK8) assay;the changes in cell migration and invasion were investigated using Transwell assay; plate colony forming test was used to evaluate the adhesion and colony forming activity of the cells. Western blotting was used to analyze the changes in the expressions of the related pathway markers. Results The relative expression of CTHRC1 mRNA in the cancer tissue specimens was 0.0411 ± 0.054, significantly higher than that in the adjacent tissues (P=0.016); this result was consistent with that of the protein assay. SW620 and LoVo cells showed obviously higher expressions of CTHRC1 than HT29 and SW480 cells at both mRNA and protein levels. LoVo cells transfected with CTHRC1 shRNA exhibited significantly suppressed proliferation, migration, invasion and colony-forming ability (P<0.05) and lowered expression of phosphorylated ERK1/2 (P-ERK1/2), but the expression of total ERK1/2 showed no obvious changes. CTHRC1 inhibition caused reverse epithelial-mesenchymal transition LoVo cells shown by increased E-cadherin expression and decreased expressions of N-cadherin, vimentin, andβ-catenin. Conclusion CTHRC1 is up-regulated in colorectal cancer tissues and SW620 and LoVo cells to promote the cell proliferation, migration, invasion and colony formation. CTHRC1 can enhance epithelial-mesenchymal transition of colorectal cancer cells by activating ERK1/2 to promote tumor cell metastasis and invasion.

Objective To explore the expression of collagen triple helix repeat containing 1 (CTHRC1) in colorectal cancer and study its role in regulating the biological behaviors of colorectal cancer LoVo cells in vitro. Methods Real-time PCR and Western blotting were used to detect the expressions of CTHRC1 in colorectal cancer tissue and paired adjacent nontumorous tissue and in 5 colorectal cancer cells. pGPU6-CTHRC1-shRNA was transfected into LoVo cells and the changes in cell proliferation was assessed using cell counting kit-8 (CCK8) assay;the changes in cell migration and invasion were investigated using Transwell assay; plate colony forming test was used to evaluate the adhesion and colony forming activity of the cells. Western blotting was used to analyze the changes in the expressions of the related pathway markers. Results The relative expression of CTHRC1 mRNA in the cancer tissue specimens was 0.0411 ± 0.054, significantly higher than that in the adjacent tissues (P=0.016); this result was consistent with that of the protein assay. SW620 and LoVo cells showed obviously higher expressions of CTHRC1 than HT29 and SW480 cells at both mRNA and protein levels. LoVo cells transfected with CTHRC1 shRNA exhibited significantly suppressed proliferation, migration, invasion and colony-forming ability (P<0.05) and lowered expression of phosphorylated ERK1/2 (P-ERK1/2), but the expression of total ERK1/2 showed no obvious changes. CTHRC1 inhibition caused reverse epithelial-mesenchymal transition LoVo cells shown by increased E-cadherin expression and decreased expressions of N-cadherin, vimentin, andβ-catenin. Conclusion CTHRC1 is up-regulated in colorectal cancer tissues and SW620 and LoVo cells to promote the cell proliferation, migration, invasion and colony formation. CTHRC1 can enhance epithelial-mesenchymal transition of colorectal cancer cells by activating ERK1/2 to promote tumor cell metastasis and invasion.