OBJECTIVETo investigate the role of miR-26b in the invasion and metastasis of colorectal cancer.

METHODSData of public chip databases were extracted to analyze the relationship between miR-26b expression and lymph node metastasis. Two types of colorectal cancer cell lines, Caco2 and DLD1, were selected, and the miR-26b-high colorectal cancer cell line was constructed using the method of lentivirus infection. The effects of up-regulating miR-26b expression on the invasion and metastasis of colorectal cancer cells were analyzed by Transwell migration and invasion experiment and wound healing assay. The effect of up-regulating miR-26b expression on stem cell phenotype of colorectal cancer cells was analyzed by sphere-formation assay.

RESULTSThe microarray detection results showed that the expression of miR-26b in tumor tissues of patients with lymph node metastasis was significantly higher than those without lymph node metastasis[(12.04±0.20) vs. (11.31±0.19), t=2.646, P = 0.010]. In the in vitro experiment section, the Transwell experiment results showed that the number of invasive cells [(16.40±1.36) vs. (3.80±0.86), t=7.814, P=0.000] and migrating cells [(33.40±2.93) vs. (8.80±2.40), t=6.505, P=0.000] in miR-26b-high colorectal cancer cells was significantly higher as compared to miR-26b-low cells(all P<0.05). Would healing assay also confirmed that the migration speed of miR-26b-high colorectal cancer cells was significantly accelerated. Both the rate and the density of sphere formation were higher in miR-26b-high colorectal cancer cells than those in miR-26b-low colorectal cancer cells [Caco2:(168.3±11.7) vs. (54.2±10.8), t=7.185,P=0.002; DLD1:(4 076.0±409.8) vs.(1 613.0±210.1), t=5.349, P=0.006].

CONCLUSIONmiR-26b may promote the invasion and metastasis of colorectal cancer by accelerating the migration and invasion of colorectal cancer cells and enhancing the stem cell phenotype of tumor cells.