ArticleJournal of cellular physiology2018
MicroRNA-16 functions as a tumor-suppressor gene in oral squamous cell carcinoma by targeting AKT3 and BCL2L2.
Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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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.
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Who cites it
26 citing papers in PubMed, 53 citations in OpenAlex.
- Natural compounds targeting miRNAs: a novel approach in oral cancer therapy.Functional & integrative genomics · 2024Review
- Eupatilin ameliorates postmenopausal osteoporosis via elevating microRNA-211-5p and repressing Janus kinase 2/Signal transducer and activator of transcription 3 pathway.Molecular and cellular biochemistry · 2024Article
- The roles and mechanisms of coding and noncoding RNA variations in cancer.Experimental & molecular medicine · 2024Review
- The impact of COVID-19 on microRNA and CD marker expression in AML patients.Scientific reports · 2024Article
- Molecular and Therapeutic Roles of Non-Coding RNAs in Oral Cancer-A Review.Molecules (Basel, Switzerland) · 2024Review
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- Molecular mechanisms of microRNA-216a during tumor progression.Cancer cell international · 2023Review
- Promising Biomarkers in Head and Neck Cancer: The Most Clinically Important miRNAs.International journal of molecular sciences · 2022Review
- Role of LINC01133 in Osteogenic Differentiation of Dental Pulp Stem Cells by Targeting miR-199b-5p.Oral health & preventive dentistry · 2022Article
- The upregulation of oncogenic miRNAs in swabbed samples obtained from oral premalignant and malignant lesions.Clinical oral investigations · 2022Article
- Epigenetic Regulations of Perineural Invasion in Head and Neck Squamous Cell Carcinoma.Frontiers in genetics · 2022Review
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- Downregulation of lncRNA MIR181A2HG by high glucose impairs vascular endothelial cell proliferation and migration through the dysregulation of the miRNAs/AKT2 axis.International journal of molecular medicine · 2021Article
- MicroRNAs as Modulators of Oral Tumorigenesis-A Focused Review.International journal of molecular sciences · 2021Review
- Overexpression of miR125b Promotes Osteoporosis Through miR-125b-TRAF6 Pathway in Postmenopausal Ovariectomized Rats.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Silencing long non-coding RNA CASC9 inhibits colorectal cancer cell proliferation by acting as a competing endogenous RNA of miR-576-5p to regulate AKT3.Cell death discovery · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant expressions of microRNAs have been reported to be strongly associated with the progression and prognosis of various tumors, including oral squamous cell carcinoma (OSCC). Recent studies on miRNA expression profiling have suggested that microRNA-16 (miR-16) may be dysregulated in OSCC. However, the tumorigenic roles and mechanisms of miR-16 in OSCC are still largely unknown. In this study, we demonstrated that miR-16 was specifically downregulated in both OSCC patients and cancer cell lines. In addition, functional roles of miR-16 in vitro suggested that the miR-16 mimic inhibited cell proliferation and induced apoptosis, whereas miR-16 inhibitor displayed the opposite effects. Luciferase reporter assay and correlation analysis showed that AKT3 and BCL2L2 were directly targeted by miR-16 and were inversely expressed with miR-16 in OSCC. Moreover, restoration of AKT3 and BCL2L2 expression could partially reverse the cell proliferation inhibition and apoptosis induction caused by miR-16. In xenograft nude mice, miR-16 mimics decreased the expression of AKT3 and BCL2L2 and reduced the tumors volumes and weights, whereas the miR-16 inhibitor exhibited adverse effects in the derived xenografts. In conclusion, the findings suggested that miR-16 functions as a tumor suppressor miRNA to inhibit cell proliferation and induce apoptosis in OSCC through decreasing the oncogenes AKT3 and BCL2L2 and that miR-16 could be a potential therapeutic target for OSCC.
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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 Socratic graph.