Abstract
Background and Aims MicroR-23b-3p (miR-23b-3p) has been found to be abnormally expressed in a variety of malignant tumors and to play a role in tumor inhibition or promotion. However, the regulatory mechanism of miR-23b-3p in COAD remains unclear. The purpose of this study was to investigate the clinical significance of miR-23b-3p expression in COAD cells and to explore its role and regulatory mechanism in the growth of COAD. Materials and Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure miR-23b-3p expression in COAD tissues and cell lines. After transfecting miR-23b-3p mimics into two human COAD cell lines (SW620 and LoVo), the cell counting kit-8 (CCK-8), colony formation, and 5-ethynyl-2′-deoxyuridine (EdU) assays were used to detect cell proliferation, the Transwell assay was used to measure cell migration and invasion capacity, and flow cytometry was used to evaluate cell apoptosis in vitro. In addition, a luciferase reporter assay was used to determine whether miR-23b-3p targets NFE2L3. The downstream regulatory mechanisms of miR-23b-3p action in COAD cells were also investigated. For in vivo tumorigenesis assay, COAD cells stably overexpressing miR-23b-3p were injected subcutaneously into the flank of nude mice to obtain tumors. Results Significantly decreased expression of miR-23b-3p was detected in COAD tissues and cell lines. Exogenous miR-23b-3p expression inhibited cell proliferation, migration, and invasion and promoted cell apoptosis of COAD cells in vitro. Nuclear factor erythroid 2 like 3 (NFE2L3) was identified as a direct target gene of miR-23b-3p. In addition, reintroduction of NFE2L3 partially abolished the anticancer effects of miR-23b-3p on COAD cells. Furthermore, miR-23b-3p overexpression hindered the growth of COAD cells in vivo. Conclusion miR-23b-3p inhibited the oncogenicity of COAD cells in vitro and in vivo by directly targeting NFE2L3, suggesting the importance of the miR-23b-3p/NFE2L3 pathway in the development of COAD.
Highlights
Colon adenocarcinoma (COAD) is a common malignant tumor with high mortality rate [1]
Expression of miR-23b-3p Is Decreased in COAD Tissues and Cell Lines. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis was performed to determine the miR-23b-3p expression level in COAD tissues and adjacent normal colon tissues. e results showed that the expression level of miR-23b-3p was notably lower in COAD tissues (Figure 1(a))
The data obtained from qRT-PCR analysis of the COAD cell lines revealed that miR-23b-3p was frequently downregulated in all four COAD cell lines (SW620, SW1116, CW-2, and LoVo) relative to its expression in normal colonic epithelial NCM460 cells (Figure 1(d))
Summary
Colon adenocarcinoma (COAD) is a common malignant tumor with high mortality rate [1]. The main methods for the clinical diagnosis of colon cancer include the fecal occult blood test, serum carcinoembryonic antigen detection, digital rectal examination, colonoscopy, and three-dimensional reconstruction of colon computed tomography (CT) [4, 5]. These methods have various disadvantages, such as low sensitivity, poor specificity, high cost, and invasiveness. Many studies have shown that the expression of certain miRNAs in tumor tissues is dysregulated in a variety of solid cancer patients, which is closely associated with tumor development, invasion, metastasis, prognosis, and drug resistance [20]. The precise roles and underlying molecular mechanisms of miR-23b-3p in COAD were elucidated
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