» Articles » PMID: 30197522

MiRNA-16 Inhibited Oral Squamous Carcinoma Tumor Growth in Vitro and in Vivo Via Suppressing Wnt/β-catenin Signaling Pathway

Overview
Publisher Dove Medical Press
Specialty Oncology
Date 2018 Sep 11
PMID 30197522
Citations 6
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Oral carcinoma, one of the most commonly diagnosed cancers, has a poor prognosis and low survival rate with treatment. In recent years, some studies reported the upregulation of miRNA-16 (miR-16) in the oral carcinoma, whereas some other studies confirmed the downregulation of miR-16. In the current study, we aimed to investigate the function of miR-16 in oral carcinoma.

Materials And Methods: Cell proliferation assay was measured by MTT assay, quantitative real time polymerase chain reaction (qRT-PCR) was used to evaluate the expression of miR-16, and apoptosis was analyzed by flow cytometry. In addition, the expression of proteins was detected by Western blot. Moreover, xenograft tumor model was established to detect the effect of miR-16 in vivo.

Results: The results suggested that miR-16 was downregulated in the oral carcinoma tissues. Overexpression of miR-16 inhibited the growth and proliferation of oral squamous carcinoma cells (OSCCs) and induced apoptosis both in vitro and in vivo, which is due to the suppression of Wnt/β-catenin signaling pathway.

Conclusion: This study provides evidence that overexpression of miR-16 inhibits OSCC growth by regulating Wnt/β-catenin signaling. Our findings suggest that overexpression of miR-16 could be a potential approach for gene therapy of OSCC in future.

Citing Articles

The role of miR-16 and miR-34a family in the regulation of cancers: A review.

Sadeghi Z, Malekzadeh M, Sharifi M, Hashemibeni B Heliyon. 2025; 11(4):e42733.

PMID: 40061926 PMC: 11889592. DOI: 10.1016/j.heliyon.2025.e42733.


Integrated analysis of gene expressions and targeted mirnas for explaining crosstalk between oral and esophageal squamous cell carcinomas through an interpretable machine learning approach.

Yadav K, Hasija Y Med Biol Eng Comput. 2024; 63(2):483-495.

PMID: 39384707 DOI: 10.1007/s11517-024-03210-z.


Review of Disease-Specific microRNAs by Strategically Bridging Genetics and Epigenetics in Oral Squamous Cell Carcinoma.

Gintoni I, Vassiliou S, Chrousos G, Yapijakis C Genes (Basel). 2023; 14(8).

PMID: 37628629 PMC: 10454361. DOI: 10.3390/genes14081578.


Salivary miR-30c-5p as Potential Biomarker for Detection of Oral Squamous Cell Carcinoma.

Mehterov N, Vladimirov B, Sacconi A, Pulito C, Rucinski M, Blandino G Biomedicines. 2021; 9(9).

PMID: 34572265 PMC: 8465705. DOI: 10.3390/biomedicines9091079.


LINC00662 Promotes Oral Squamous Cell Carcinoma Cell Growth and Metastasis through miR-144-3p/EZH2 Axis.

Yao Y, Liu Y, Jin F, Meng Z Yonsei Med J. 2021; 62(7):640-649.

PMID: 34164962 PMC: 8236341. DOI: 10.3349/ymj.2021.62.7.640.


References
1.
Saito-Diaz K, Chen T, Wang X, Thorne C, Wallace H, Page-McCaw A . The way Wnt works: components and mechanism. Growth Factors. 2012; 31(1):1-31. PMC: 3697919. DOI: 10.3109/08977194.2012.752737. View

2.
Huang S, Zou X, Zhu J, Fu Y, Lin Q, Liang Y . Attenuation of microRNA-16 derepresses the cyclins D1, D2 and E1 to provoke cardiomyocyte hypertrophy. J Cell Mol Med. 2015; 19(3):608-19. PMC: 4369817. DOI: 10.1111/jcmm.12445. View

3.
Toda T, Homma D, Tokuoka H, Hayakawa I, Sugimoto Y, Ichinose H . Birth regulates the initiation of sensory map formation through serotonin signaling. Dev Cell. 2013; 27(1):32-46. DOI: 10.1016/j.devcel.2013.09.002. View

4.
Li Z, Yu X, Shen J, Jiang Y . MicroRNA dysregulation in uveal melanoma: a new player enters the game. Oncotarget. 2015; 6(7):4562-8. PMC: 4467099. DOI: 10.18632/oncotarget.2923. View

5.
Chen F, Chen L, He H, Huang W, Zhang R, Li P . Up-regulation of microRNA-16 in Glioblastoma Inhibits the Function of Endothelial Cells and Tumor Angiogenesis by Targeting Bmi-1. Anticancer Agents Med Chem. 2015; 16(5):609-20. DOI: 10.2174/1871520615666150916092251. View