AI Article Synopsis
- miR-23b-3p is found to be significantly less expressed in colorectal cancer (COAD) tissues and cell lines, indicating its potential role in tumor suppression.
- In lab experiments, introducing miR-23b-3p led to reduced cell growth, migration, and invasiveness, alongside increased cell death in COAD cells; NF-E2-related factor 2 (Nrf2) was identified as its direct target.
- The study concludes that miR-23b-3p plays a crucial role in inhibiting COAD progression both in vitro and in vivo, emphasizing its importance as a potential therapeutic target.
Article 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 . 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 () was identified as a direct target gene of miR-23b-3p. In addition, reintroduction of 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 , suggesting the importance of the miR-23b-3p/NFE2L3 pathway in the development of COAD.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8712119 | PMC |
| http://dx.doi.org/10.1155/2021/8493225 | DOI Listing |
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