Circ_0056618 enhances PRRG4 expression by competitively binding to miR-411-5p to promote the malignant progression of colorectal cancer.

Abstract

The purpose of this paper was to explore the role of circ_0056618 and associated mechanisms in colorectal cancer (CRC). The expression of circ_0056618, proline rich and Gla domain 4 (PRRG4) mRNA and miR-411-5p was measured by quantitative real-time PCR (qPCR).The protein levels of PRRG4 and epithelial-mesenchymal transition (EMT)-related markers were detected by western blot. Cell proliferation was assessed by cell counting kit-8, EdU, and colony formation assays. Cell migration and invasion were assessed by transwell assay. Cell apoptosis was detected by flow cytometry assay. The putative relationship between miR-411-5p and circ_0056618 or PRRG4 was verified by dual-luciferase reporter assay. The effects of circ_0056618 on tumor growth in vivo were determined by animal study. Circ_0056618 and PRRG4 was upregulated, while miR-411-5p was downregulated in CRC tumor tissues and cells. Circ_0056618 knockdown or PRRG4 knockdown inhibited CRC cell proliferation, migration/invasion, EMT, and survival. Circ_0056618 positively modulated PRRG4 expression by targeting miR-411-5p. MiR-411-5p absence or PRRG4 overexpression could rescue circ_0056618 knockdown-induced inhibition on proliferation, migration/invasion, and EMT in CRC cells. Animal assay showed circ_0056618 knockdown impeded tumor growth in vivo. Circ_0056618 promoted CRC growth and development by upregulating PRRG4 expression via competitively targeting miR-411-5p.