lncRNA SNHG22 sponges miR‑128‑3p to promote the progression of colorectal cancer by upregulating E2F3

Abstract

The long non‑coding RNA (lncRNA) small nucleolar RNA host gene 22 (SNHG22) has been reported as a crucial regulator in several types of human cancer. The present study evaluated the function and mechanism of SNHG22 in colorectal cancer (CRC) progression. SNHG22 expression was detected in colorectal adenoma, CRC tumor tissues (TTs) and adjacent non‑cancerous tissues (ANTs) using reverse transcription‑quantitative PCR (RT‑qPCR). The biological behaviors of SNHG22 in CRC cell lines were explored <em>in vitro</em> using Cell Counting Kit‑8, flow cytometry, wound scratch assay and Transwell assay, and <em>in vivo</em> using a nude mouse xenograft model. The interaction between SNHG22 and microRNA‑128‑3p (miR‑128‑3p), and the target genes of miR‑128‑3p were explored using online tools, RT‑qPCR, western blotting and a dual‑luciferase reporter assay. The present study revealed that SNHG22 expression was most highly expressed in TTs followed by adenoma tissues and ANTs. In addition, high <em>SNHG22</em> expression levels were significantly associated with advanced clinicopathological factors and worse survival in patients with CRC. <em>SNHG22</em> knockdown markedly inhibited CRC cell proliferation, apoptosis resistance, migration and invasion <em>in vitro</em>, and hindered tumor growth <em>in vivo</em>. The mechanistic study revealed that SNHG22 bound to miR‑128‑3p and attenuated its inhibitory effects on E2F transcription factor 3 (E2F3) expression levels and activity. Rescue experiments demonstrated that inhibiting miR‑128‑3p or upregulating E2F3 offset the effects of <em>SNHG22</em> knockdown on CRC cells. The present findings support the existence of an interactive regulatory network involving SNHG22, miR‑128‑3p and E2F3 in CRC cell lines, indicating that the SNHG22/miR‑128‑3p/E2F3 axis may be considered a novel diagnostic and therapeutic target in CRC.

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