Hypomethylation-mediated LINC00346 facilitates cell phenotype progression of colon adenocarcinoma via modulating miR-589-5p/CCL5

Abstract

The study aimed to investigate the role of LINC00346 in colon adenocarcinoma (COAD) metastasis. qRT-PCR, methylation-specific PCR, immunohistochemistry and western blotting were used to measure the expression levels of LINC00346, miR-589–5p, and CCL5 in COAD cells and tissues. Dual-luciferase assays, RNA immunoprecipitation, and RNA pull-down were used to validate the targeting relationship between LINC00346/CCL5 and miR-589–5p. In vivo experiments were conducted to study the impact of LINC00346 on COAD progression. MTT, colony formation assay, transwell assay and wound healing assay were used to detect the COAD cell proliferation, colony formation, invasion and migration. The results showed that COAD cells and tissues had high expression of LINC00346 and CCL5, and low expression of miR-589–5p. LINC00346 expression was upregulated due to DNA hypomethylation in its promoter region. miR-589–5p targets both LINC00346 and CCL5. LINC00346 facilitated the malignant progression of COAD by preventing the degradation of CCL5 via competitively binding to miR-589–5p. Rescue experiments indicated a ceRNA pattern consisting of LINC00346, miR-589–5p, and CCL5. Overall, LINC00346 promotes COAD progression via the miR-589–5p/CCL5 axis and may be a potential therapeutic target for COAD.