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 in vitro using Cell Counting Kit-8, flow cytometry, wound scratch assay and Transwell assay, and in vivo 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 SNHG22 expression levels were significantly associated with advanced clinicopathological factors and worse survival in patients with CRC. SNHG22 knockdown markedly inhibited CRC cell proliferation, apoptosis resistance, migration and invasion in vitro , and hindered tumor growth in vivo . 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 SNHG22 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.

Cross-Talk Between m6A- and m5C-Related lncRNAs to Construct a Novel Signature and Predict the Immune Landscape of Colorectal Cancer Patients

“…Luan and colleagues recently reported that ALMS1-IT1 promoted the malignant progression of lung adenocarcinoma through AVL9-mediated activation of the cyclindependent kinase pathway (73). SNHG22 has been detected to be overexpressed and to act as an oncogene in multiple cancers, including CRC (74,75). Yao et al (75) revealed that SNHG22 promoted CRC cell growth, migration, and invasion through SNHG22/miR-128-3p/E2F3 axis.…”

“…SNHG22 has been detected to be overexpressed and to act as an oncogene in multiple cancers, including CRC (74,75). Yao et al (75) revealed that SNHG22 promoted CRC cell growth, migration, and invasion through SNHG22/miR-128-3p/E2F3 axis. LINC00628 has been reported to inhibit the malignant progression of cancer through different mechanisms, such as binding to EZH2 to regulate the p57 or H3K27me3 level (76,77), and interacting with the promoter of LAMA3 or VEGFA (78,79).…”

AFF3 is a novel prognostic biomarker and a potential target for immunotherapy in gastric cancer

“… 19 In addition, the density of infiltrated immune cells also has a crucial effect on patients’ prognosis in a variety of cancers; the presence of stromal cells and other immune cells have a strong correlation with the prognosis of multiple cancer. 37 , 38 , 39 Additionally, growing studies have shown that the high immune/stromal/estimate score is an independent prognostic factor(s) for poor overall survival of GC. 3 , 25 , 40 , 41 In our study, the overexpression of AFF3 was positively correlated with the high immune/stromal/estimate.…”

circFIG 4 drives the carcinogenesis and metastasis of esophagus cancer via the miR‐493‐5p/E2F3 axis

“…The interaction of miRNAs and E2F3 in regulating human cancers was proposed, and E2F3 was verified to exert a carcinogenic role in diverse tumors. 27 For instance, lncRNA SNHG22 could accelerate the development of colorectal cancer by sponging miR-128-3p and upregulating E2F3 expression, 28 and miR-573 suppressed cell progression in pancreatic cancer through regulating E2F3. 29 Likewise, E2F3 had elevated levels in esophageal squamous cell carcinoma (ESCC), and circ_0087378 deficiency blocked ESCC cell progression by enhancing E2F3 expression.…”