Promotes Colon Cancer Cell Proliferation by Targeted Expression Inhibitionn.

OBJECTIVE

Colon cancer (CC) is the third most common cancer with a high rate of incidence and mortality. Therefore, it is highly necessary to explore novel targets of CC.

METHODS

The miRNA-seq and RNA-seq data of CC were accessed from the TCGA database. Differential analysis was performed using the "edgeR" package to identify differentially expressed miRNAs (DE_miRNAs). The downstream target genes of the target miRNA were then predicted by miRNA target prediction databases to identify the target mRNA. Normal colon cell line CCD-18Co and CC cell lines HCT-116, HT-29, SW620 and SW480 were chosen, and qRT-PCR was conducted to detect expression in these cell lines. qRT-PCR and Western blot were carried out to determine mRNA and protein expression, respectively. Dual-luciferase reporter gene assay was performed to verify the targeting relationship between and 3'UTR. CCK-8 assay and colony formation assay were carried out to detect cell proliferation. Meanwhile, tumor xenograft model in nude mice was constructed to assess CC cell tumorigenic ability in vivo.

RESULTS

was markedly up-regulated in CC tissue. CC cell proliferation and in vivo tumorigenic ability were suppressed by silencing but promoted by over-expression. was significantly down-regulated in cancer tissue. Dual-luciferase reporter gene assay indicated that could bind to 3'UTR. expression was noticeably elevated upon deficiency but significantly inhibited upon over-expression. CCK-8 and colony formation assay suggested that facilitated CC cell proliferation by silencing .

CONCLUSION

promotes CC cell proliferation by targeted silencing .