A number of
cancers show increased expression of
paxillin which plays a central role in
tumor progression, including
colorectal cancer. However, the mechanisms causing
paxillin upregulation remains unclear. In our study, bioinformatics analyses suggested that
paxillin is predicted to be a direct target of miR-145. We firstly identified
paxillin as a new target of miR-145 and demonstrated that miR-145 inhibits
paxillin expression by binding to the
paxillin mRNA 3'UTR. Therefore, we assume overexpression of
paxillin induced by suppression of miR-145 may promote cell migration and invasion. We detected the expression of
paxillin and miR-145 in human
colorectal cancer tissues by real-time quantitative PCR. Higher expression of
paxillin and lower expression of miR-145 was observed in
colorectal cancer tissues than corresponding paracancerous tissue. Moreover, the expression of
paxillin was negatively correlated with miR-145 expression. A dual-
luciferase reporter assay was used to confirm that
paxillin was a direct target of miR-145. In CRC cell lines, overexpression of miR-145 could downregulate
paxillin protein expression levels, and ectopic overexpression of miR-145 mimics or inhibitor could inhibit or promote cell migration, invasion, proliferation and clone formation in vitro. Taken together, these data suggested that miR-145 plays a pivotal role in
colon cancer through inhibiting cell proliferation migration and invasion, and miR-145 may serve as a
tumor suppressor by targeting
paxillin gene.