ArticleOncology letters2018
miR-371-5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Astaxanthin suppresses the malignant behaviors of nasopharyngeal carcinoma cells by blocking PI3K/AKT and NF-κB pathways via miR-29a-3p.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2024Article
- MiR-371a-5p Positively Associates with Hepatocellular Carcinoma Malignancy but Sensitizes Cancer Cells to Oxaliplatin by Suppressing BECN1-Dependent Autophagy.Life (Basel, Switzerland) · 2022Article
- PPARβ/δ Agonist GW501516 Inhibits Tumorigenesis and Promotes Apoptosis of the Undifferentiated Nasopharyngeal Carcinoma C666-1 Cells by Regulating miR-206.Oncology research · 2019Article
- microRNA-29a functions as a tumor suppressor in nasopharyngeal carcinoma 5-8F cells through targeting VEGF.Iranian journal of basic medical sciences · 2019Article
- The Role of MicroRNAs in Recurrence and Metastasis of Head and Neck Squamous Cell Carcinoma.Cancers · 2019Review
- The regulatory network of nasopharyngeal carcinoma metastasis with a focus on EBV, lncRNAs and miRNAs.American journal of cancer research · 2018Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the expression and function of microRNA (miR)-371-5p in nasopharyngeal carcinoma (NPC). The levels of miR-371-5p were analyzed in nasopharyngeal epithelium tissues, NPC tissues, human NPC cell lines and NP69 cells using reverse transcription-quantitative polymerase chain reaction analysis. The association between the level of miR-371-5p and clinicopathological variables was also investigated. Cell proliferation was determined using an MTT assay, and the activities of cell metastasis were determined using wound healing and Transwell migration assays. To assess whether miR-371-5p can combine with the targeting sequence of B-cell lymphoma 2 (BCL2) mRNA or not, a luciferase activity assay was performed. An animal experiment was used to examine the effect of miR-371-5p on the development of NPC. The results revealed that the expression of miR-371-5p was reduced in NPC samples and NPC cells. The level of miR-371-5p was associated with clinical stage and distant metastasis in patients with NPC, and was inversely associated with the protein level of BCL-2 in NPC tissues. The upregulation of miR-371-5p reduced cell growth, migration and invasion, and inhibited carcinoma growth through targeting BCL2 mRNA. Taken together, the regulation of miR-371-5p was shown to offer potential as a novel treatment approach for NPC.
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