ArticleInternational journal of clinical and experimental pathology2017
MicroRNA-140 inhibits tumor progression in nasopharyngeal carcinoma by targeting CXCR4.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- MiRNA signatures in nasopharyngeal carcinoma: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2023Review
- Aberrant regulation of CXCR4 in cancer via deviant microRNA-targeted interactions.Epigenetics · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence has indicated that miRNAs play important roles in carcinogenesis. The identification of dysregulated miRNAs and the target genes they regulate might enhance our understanding of the molecular mechanisms of nasopharyngeal carcinoma (NPC). microRNA-140 (miR-140) has been found to be down-regulated in cancer. However its role in nasopharyngeal carcinoma remains unclear. CXCR4 was predicted to be the target gene of miR-140. The current research was designed to delineate the mechanism of miR-140 in regulating NPC via targeting CXCR4. In this study, miR-140 was underexpressed in NPC tissues and cell lines compared with their normal controls and the biological function and direct target genes of miR-140 in NPC cells were investigated. Importantly, we demonstrate that the over expression of miR-140 significantly inhibits NPC cell proliferation and induces apoptosis. Additionally, CXCR4 was predicted the target gene of miR-140 and the luciferase reporter assay revealed that miR-140 was directly bound to the 3'-UTR of CXCR4. Furthermore, CXCR4 was inversely correlated with the expression of miR-140 in NPC cells. Taken together, our results suggest miR-140 suppresses tumor proliferation and induces apoptosis by inhibiting CXCR4, which might provide a new insight into the molecular mechanisms that regulate the development and progression of NPC, and it provides novel therapeutic targets for NPC.
Indexed as
Identifiers
31966622PMC6965283W3028382749What OpenQuestion holds
Registered trials
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 OpenQuestion graph.