Abstract: Objective:To investigate the expression of miR-92a in colorectal cancer (CRC) and its effect on the regulation mechanisms of tumor angiogenesis. Methods:The miRNA- 92a expression in25CRC tissues and HT 29, SW 620 , SW 480 , and HCT116 CRC cells was detected using quantitative real- time polymerase chain reaction. The CD31positive expression of blood microvessels in CRC tissues was measured by immunohistochemistry. Pearson correlation analysis was used to analyze the relationship between miR- 92a and tu-mor angiogenesis. The miR-92a mimic or inhibitor was transfected into HCT 116 and SW620 cells in vitro to upregulate or downregu-late the miR- 92a expression. The effect of miR- 92a overexpression or suppression on the formation of human umbilical vein endotheli-al cell (HUVEC) tubules was detected by tube formation assay. Changes in phosphatase and tensin homolog (PTEN) protein expression were measured by Western blot.Results:The expression level of miR- 92a in CRC tissues was significantly higher than that in matched adjacent tissues (P<0. 01). The expression levels of miR- 92a in HT 29, SW 480 , SW 620 , and HCT116 colon cancer cell lines were signifi-cantly higher than that of the normal colorectal epithelium control (P<0. 05). The number of CD 31positive expression of microvessel density (MVD) in CRC tissues was significantly higher than that in adjacent tissues ( P<0. 01), and the miR-92a expression level was posi -tively correlated with the MVD in CRC tissues (r=0. 580 , P=0. 01). The cell culture supernatant of HCT 116 with miR- 92a overexpression could significantly promote the formation of HUVEC tubules ( P<0. 05). The upregulation of miR- 92a expression could significantly inhib -it the expression of PTEN protein in CRC cells (P<0. 01). Conclusion: The miR- 92a was highly expressed in CRC cells and tissues, which was closely related to the formation of tumor angiogenesis in CRC. The miR-92a could promote tumor angiogenesis in CRC by inhibit-ing PTEN expression.