Abstract:

Objective To explore the molecular mechanism that miRNA ⁃26b ⁃5p（miR ⁃26b ⁃5p）targets the expression level of NFE2L3 and affects the growth，migration，and invasion of colorectal cancer cells. Methods The expression levels of miR⁃26b⁃5p in human normal intestinal epithelial cells（NCM460）and colorectal cancer cell lines（HT29，SW620 and HCT116）were detected by qPCR. The expression level of NFE2L3 in the above cell lines was detected by qPCR and western blot. Bioinformatics methods analyzed the target sequence of miRNA⁃26b⁃ 5p binding to NFE2L3. The dual luciferase gene reporter experiment detects the targeted regulation mechanism of miR⁃26b⁃5p on NFE2L3. Liposome method was used to transfect miR⁃26b⁃5p mimic or NFE2L3 into HT29 and SW620 colorectal cancer cell lines，to observe the effect on cell growth through CCK⁃8 and clone formation experiment，to observe cell apoptosis by flow cytometry and to observe cell migration and invasion through Transwell assay. Results Compared with human normal epithelial cell lines，the expression level of miR⁃26b⁃5p in colorectal cancer cell lines was significantly down⁃regulated（P < 0.05），while the mRNA and protein levels of NEF2L3 were significantly up⁃regulated（P < 0.05）. The dual luciferase gene reporter experiment showed that miR⁃26b⁃5p can significantly affect the luciferase activity of NEF2L3 3′UTR expression vector（P < 0.05）. Overexpression of miR⁃ 26b⁃5p significantly inhibited the growth，colony formation，migration and invasion of colorectal cancer cell lines， and induce cell apoptosis（all P < 0.05），while overexpression of NEF2L3 can counteract the effects of miR⁃26b⁃5p （all P < 0.05）. Conclusion In colorectal cancer ，miR⁃26b⁃5p is lowly expressed ，while NEF2L3 is highly expressed；miR ⁃26b ⁃5p can target and regulate the expression level of oncogene EF2L3，thereby regulating the growth，apoptosis，migration and invasion of colorectal cancer cells，thereby participating in the tumorigenesis and development of colorectal cancer.

Key words:

miR?26b?5p, NEF2L3, colorectal cancer, growth, apoptosis, migration, invasion