MiR-211-5p Inhibits the Biological Behaviors of Colorectal Cancer via SPARC-Related Growth Factor Pathways.

Abstract

Colorectal cancer (CRC) is a highly malignant cancer with poor prognosis. MiR-211-5p has been widely studied as an antioncogene; however, its function and mechanism in CRC are still unknown. This study aimed to investigate the expression patterns and biological implications of miR-211-5p in CRC. This study used quantitative real-time polymerase chain reaction to evaluate miR-211-5p expression in CRC cells and tissues. MiR-211-5p mimics were constructed to overexpress miR-211-5p in Lovo and SW480 cells. Tumor bioactivities of CRC, including cell proliferation, migration, invasion, and colony formation, were evaluated. The dual-luciferase assay was used to confirm the targeted relationship between miR-211-5p expression and secreted protein acidic and rich in cysteine (SPARC). In addition, Western blot analysis and immunohistochemical staining were used to measure SPARC, platelet-derived growth factor (PDGF), transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF) expression levels. This study showed downregulated miR-211-5p expression in CRC cells and tissues, and this downregulation correlated with CRC progression. Meanwhile, miR-211-5p restrained CRC cell proliferation, colony formation, migration, and invasion. Mechanistically, SPARC-related growth factor pathways, including VEGF, PDGF, and TGF-β pathways, were upregulated in CRC tissues. Furthermore, SPARC acted as the target gene for miR-211-5p. Finally, SPARC overexpression suppressed the inhibitory effect of miR-211-5p on CRC cell progression. MiR-211-5p suppressed the invasion, migration, proliferation, and progression of CRC cells through sponging SPARC-related growth factor pathways.