ArticleOncology letters2018
MiR-34c induces apoptosis and inhibits the viability of M4e cells 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 8 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.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Protective Role of miR-34c in Hypoxia by Activating Autophagy through BCL2 Repression.Molecules and cells · 2022Article
- Article
- Noncoding RNAs in apoptosis: identification and function.Turkish journal of biology = Turk biyoloji dergisi · 2022Review
- MiRNA-34c Regulates Bovine Sertoli Cell Proliferation, Gene Expression, and Apoptosis by Targeting theAnimals : an open access journal from MDPI · 2021Article
- MicroRNA-212-5p and its target PAFAH1B2 suppress vascular proliferation and contraction via the downregulation of RhoA.PloS one · 2021Article
- Up-regulation of miR-34c-5p inhibits nasopharyngeal carcinoma cells by mediating NOTCH1.Bioscience reports · 2020Article
- miR-185-5p response to usnic acid suppresses proliferation and regulating apoptosis in breast cancer cell by targeting Bcl2.Biological research · 2020Article
- The Expression of miR-34c-5p Induces G0/G1 Cell Cycle Arrest and Apoptosis in SW480 Colon Cancer Cell.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate microRNA (miR/miRNA)-34c expression and the association of miR-34c with B cell lymphoma 2 (BCL2) in M4e laryngeal carcinoma cell line. M4e laryngeal carcinoma cells were cultured and transfected with lenti-miR-34c or scramble miRNA for 72 h. Cell viability and the percentage of cells undergoing apoptosis of transfected cells were detected using MTT and Annexin V/allophycocyanin and propidium iodide assays, respectively. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were performed to determine BCL2 mRNA and protein expression in transfected M4e cells. In addition, luciferase reporter assay was performed to identify whether BCL2 is a direct target of miR-34c. Transfection of lenti-miR-34c was able to significantly inhibit cell viability (P<0.01), increase the percentage of cells undergoing apoptosis (P<0.001) and downregulate BCL2 protein expression (P<0.01) in M4e cells. RT-qPCR data revealed that lenti-miR-34c transfection did not affect BCL2 mRNA expression. However, data from the luciferase reporter assay revealed that transfection with miR-34c negative control decreased luciferase activity in M4e cells co-transfected with pGL3-BCL2-MUT plasmid, compared with miR-34c inhibitor (P<0.01). Collectively, the results from the present study provided evidence that miR-34c may be involved in the pathogenesis of laryngeal cancer, and BCL2 may be negatively regulated by miR-34c in M4e cells.
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