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. 2020 Jun;9(11):3954-3963.
doi: 10.1002/cam4.3002. Epub 2020 Apr 11.

Long noncoding RNA MEG3 decreases the growth of head and neck squamous cell carcinoma by regulating the expression of miR-421 and E-cadherin

Yefeng Ji  1 , Guanying Feng  1 , Yunwen Hou  1 , Yang Yu  1 , Ruixia Wang  1 , Hua Yuan  1   2
Affiliations

Long noncoding RNA MEG3 decreases the growth of head and neck squamous cell carcinoma by regulating the expression of miR-421 and E-cadherin

Yefeng Ji et al. Cancer Med. 2020 Jun.

Abstract

Background: Maternally expressed 3 (MEG3), a long chain noncoding RNA (lncRNA), has verified its function as a suppressor in several kinds of cancers. However, the downstream mechanism of MEG3 in regulating the molecular mechanism of epithelial-mesenchymal transformation (EMT) in head and neck squamous cell carcinoma (HNSCC) progression demands further investigation.

Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression level of MEG3 in HNSCC and adjacent normal tissues of 51 cases. Luciferase report assay was used to detect the correlation between miR-421 and MEG3, and miR-421 and E-cadherin in HNSCC cell lines. Cell invasion and proliferation capacity were assessed through transwell and CCK8 assays. Scratch wound assay was used to assess cell migration capacity.

Results: Firstly, this study demonstrated that the expression of MEG3 was significantly downregulated in HNSCC compared to adjacent normal tissues. Overexpressed MEG3 inhibited cell proliferation, migration, and invasion in vitro. Secondly, MEG3 upregulated the expression of E-cadherin, which was instead downregulated by miR-421. MiR-421 was negatively regulated by MEG3 in HNSCC. Therefore, MEG3 regulated EMT by sponging miR-421 targeting E-cadherin in HNSCC.

Conclusions: This study indicated that the MEG3-miR-421-E-cadherin axis could be a new therapeutic target for HNSCC.

Keywords: epithelial-mesenchymal transition; head and neck squamous cell carcinoma; maternally expressed 3; miR-421.

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Conflict of interest statement

None.

Figures

FIGURE 1
FIGURE 1
A, The relative expression of MEG3 in 51 cases of HNSCC tissues and adjacent normal tissues in pairs. B, The relative expression of MEG3 in TCGA database. C, The relative expression of MEG3 in HNSCC cell lines Cal27, Fadu, and HN4 and oral epithelium cell (HOEC). *P < .05, **P < .01
FIGURE 2
FIGURE 2
A, The relative expression of MEG3 in Fadu and Cal27 cells transfected with empty vectors (MEG3 control) or MEG3‐overexpressed lentivirus (MEG3 overexpression). B, The invasion ability of transfected Fadu and Cal27 cells. C, The migration of transfected Fadu and Cal27 cells. D, The proliferation of transfected Fadu and Cal27 cells. *P < .05, **P < .01
FIGURE 3
FIGURE 3
MEG3 inhibited the EMT process. The relative protein levels of Vimentin, ZEB2, and E‐cadherin in transfected Fadu and Cal27 cells. *P < .05, **P < .01
FIGURE 4
FIGURE 4
A, MEG3 wild‐type and mutant plasmid. B and C, Luciferase reporter assays in 293T and Fadu cells. MiR‐421 was a target of MEG3 in HNSCC. D, The relative expression of miR‐421 in transfected Fadu and Cal27 cells. *P < .05, **P < .01
FIGURE 5
FIGURE 5
A, The invasion ability of Fadu and Cal27 cells transfected with miR‐421 mimics or inhibitors. B, The proliferation ability of transfected Fadu and Cal27 cells. *P < .05, **P < .01
FIGURE 6
FIGURE 6
A, E‐cadherin wild‐type and mutant plasmids. B and C, Luciferase reporter assays in 293T and Fadu cells. *P < .05, **P < .01
FIGURE 7
FIGURE 7
A and B, Relative E‐cadherin expression in transfected Fadu and Cal27 cells. **P < .01, *P < .05
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References

    1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019. CA Cancer J Clin. 2019;69:7‐34. - PubMed
    1. Rahimy E, Kuo SZ, Ongkeko WM. Evaluation of non‐coding RNAs as potential targets in head and neck squamous cell carcinoma cancer stem cells. Curr Drug Targets. 2014;15:1247‐1260. - PubMed
    1. Dunne S, Mooney O, Coffey L, et al. Psychological variables associated with quality of life following primary treatment for head and neck cancer: a systematic review of the literature from 2004 to 2015. Psychooncology. 2017;26:149‐160. - PubMed
    1. Zecha JAEM, Raber‐Durlacher JE, Nair RG, et al. Low‐level laser therapy/photobiomodulation in the management of side effects of chemoradiation therapy in head and neck cancer: part 2: proposed applications and treatment protocols. Support Care Cancer. 2016;24:2793‐2805. - PMC - PubMed
    1. Li X, Cao Y, Gong X, Li H. Long noncoding RNAs in head and neck cancer. Oncotarget. 2017;8:10726. - PMC - PubMed

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