ArticleCancer management and research2020
MiR-218-5p Suppresses the Progression of Retinoblastoma Through Targeting NACC1 and Inhibiting the AKT/mTOR Signaling Pathway.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Functional significance of miR-218 in lung cancer.Journal of cancer metastasis and treatment · 2026Article
- High Expression of miR-218-5p in the Peripheral Blood Stream and Tumor Tissues of Pediatric Patients with Sarcomas.Biochemical genetics · 2025Article
- NACC1 accelerates the progression of AML by regulating the ADAM9/PI3K/AKT axis.International journal of medical sciences · 2025Article
- Highly Sensitive and Specific Panels of Plasma Exosomal microRNAs for Identification of Malignant Pulmonary Nodules.The clinical respiratory journal · 2024Article
- miR-218-5p, miR-124-3p and miR-23b-3p act synergistically to modulate the expression of NACC1, proliferation, and apoptosis in C-33A and CaSki cells.Non-coding RNA research · 2024Article
- miR-4529-3p Promotes the Progression of Retinoblastoma by Inhibiting RB1 Expression and Activating the ERK Signaling Pathway.Molecular biotechnology · 2024Article
- THUMPD3-AS1 facilitates cell growth and aggressiveness by the miR-218-5p/SKAP1 axis in colorectal cancer.Cell biochemistry and biophysics · 2022Article
- miR-18a-5p derived from mesenchymal stem cells-extracellular vesicles inhibits ovarian cancer cell proliferation, migration, invasion, and chemotherapy resistance.Journal of translational medicine · 2022Article
- Hsa_circ_0050102 regulates the pancreatic cancer development via miR-218-5p/PPME1 axis.Journal of clinical laboratory analysis · 2022Article
- Role of non-coding RNAs and exosomal non-coding RNAs in retinoblastoma progression.Frontiers in cell and developmental biology · 2022Review
- circRNF20 aggravates the malignancy of retinoblastoma depending on the regulation of miR-132-3p/PAX6 axis.Open medicine (Warsaw, Poland) · 2022Article
- The Overexpression of TOB1 Induces Autophagy in Gastric Cancer Cells by Secreting Exosomes.Disease markers · 2022Article
- Long non-coding RNA HOXA-AS3 promotes cell proliferation of oral squamous cell carcinoma through sponging microRNA miR-218-5p.Bioengineered · 2021Article
- Silencing of NACC1 inhibits the proliferation, migration and invasion of nasopharyngeal carcinoma cells via regulating the AKT/mTOR signaling pathway.Oncology letters · 2021Article
- Aberrant expression of SNHG12 contributes to N, N-dimethylformamide-induced hepatic apoptosis both in short-term and long-term DMF exposure.Toxicology research · 2021Article
- A New Case ofFrontiers in pediatrics · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionMicroRNA-218-5p (miR-218-5p) was involved in the progression of multiple tumors as a tumor suppressor miRNA. Its specific role on human retinoblastoma (RB) cells remains unknown.
methodsWe constructed the miR-218-5p overexpression and knockdown cells to detect their role on RB cell line WERI-Rb-1, and we analyzed its binding sites on TargetScan. CCK8 and clonogenic assays were performed to detect cell viability. Flow cytometry was used for the detection of cell apoptosis.
resultsOur results showed that the miR-218-5p inhibitor enhanced cell viability and blocked the apoptosis in RB cells. The AKT/mTOR signaling pathway was also inhibited by the miR-218-5p inhibitor. MiR-218-5p mimics lead to diametrically opposite results. Nucleus accumbens-associated 1 (NAC1) encoded by the NACC1 gene is involved in the regulation of many biological functions, including gene transcription, protein degradation of ubiquitin pathway, cell viability, and apoptosis. In this research, dataset analysis suggested that NACC1 might be a downstream target of miR-218-5p. Then, qPCR and Western blot analysis proved that miR-218-5p inhibited the expression of NACC1 in RB cells. NACC1 could promote cell viability and inhibit the apoptosis by activating the AKT/mTOR signaling pathway. MiR-218-5p mimics blocked the enhancement of cell growth induced by NACC1 overexpression as well as the activation of the AKT/mTOR signaling pathway in RB cells. DISCUSSION: MiR-218-5p inhibited cell growth by targeting NACC1 and suppressing the AKT/mTOR signaling pathway. MiR-218-5p/NACC1/AKT/mTOR might be a new target axis for the clinical treatment strategy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.