Effect of ART1 on the proliferation and migration of mouse colon carcinoma CT26 cells in vivo

Abstract

Arginine-specific mono-ADP-ribosyltransferase 1 (ART1) is an important enzyme that catalyzes arginine-specific mono-ADP-ribosylation. There is evidence that arginine-specific mono-ADP-ribosylation may affect the proliferation of smooth muscle cells via the Rho-dependent signaling pathway. Previous studies have demonstrated that ART1 may have a role in the proliferation, invasion and apoptosis of colon carcinoma in vitro. However, the effect of ART1 on the proliferation and invasion of colon carcinoma in vivo has yet to be elucidated. In the present study, mouse colon carcinoma CT26 cells were infected with a lentivirus to produce ART1 gene silencing or overexpression, and were then subcutaneously transplanted. To observe the effect of ART1 on tumor growth or liver metastasis in vivo, a spleen transplant tumor model of CT26 cells in BALB/c mice was successfully constructed. Expression levels of focal adhesion kinase (FAK), Ras homolog gene family member A (RhoA) and the downstream factors, c-myc, c-fos and cyclooxygenase-2 (COX-2) proteins, were measured in vivo. The results demonstrated that ART1 gene silencing inhibited the growth of the spleen transplanted tumor and its ability to spread to the liver via metastasis. There was also an accompanying increase in expression of FAK, RhoA, c-myc, c-fos and COX-2, whereas CT26 cells with ART1 overexpression demonstrated the opposite effect. These results suggest a potential role for ART1 in the proliferation and invasion of CT26 cells and a possible mechanism in vivo.