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. 2020 Jul;22(7):e3184.
doi: 10.1002/jgm.3184. Epub 2020 Apr 18.

LINC00467 enhances head and neck squamous cell carcinoma progression and the epithelial-mesenchymal transition process via miR-299-5p/ubiquitin specific protease-48 axis

Ye Chen  1 , Yiying Ding  2
Affiliations

LINC00467 enhances head and neck squamous cell carcinoma progression and the epithelial-mesenchymal transition process via miR-299-5p/ubiquitin specific protease-48 axis

Ye Chen et al. J Gene Med. 2020 Jul.

Abstract

Background: Head and neck squamous cell carcinoma (HNSCC) has attracted the attention of researchers as a result of its high incidence around the world. This malignancy occurs in the oral cavity, pharynx and larynx in most cases. A number of lncRNAs have been revealed to regulate the malignant neoplasia of several cancers. Nevertheless, the effects of lncRNA LINC00467 in HNSCC have not yet been reported.

Methods: The expression of LINC00467, miR-299-5p and ubiquitin specific protease-48 (USP48) in HNSCC cells was quantified by a quantitative reverse transcriptase-polymerase chain reaction. The influences of LINC00467 deficiency on HNSCC progression were reflected by cell counting kit-8, colony formation, ethynyl-2-deoxyuridine, wound healing and western blot assays. RIP and luciferase reporter assays were conducted to confirm the interaction among LINC00467, miR-299-5p and USP48.

Results: LINC00467 was considerably upregulated in HNSCC cells, and an absence of LINC00467 suppressed cell growth, cell migration and the epithelial-mesenchymal process in HNSCC. In addition, miR-299-5p expression was notably downregulated in HNSCC cells, and miR-299-5p could bind with LINC00467. Furthermore, USP48 was conspicuously overexpressed in HNSCC cells and capable of binding with miR-299-5p. LINC00467 could upregulate USP48 expression via sponging miR-299-5p. Finally, rescue assays proved that USP48 overexpression could compensate for the suppressive effects on HNSCC progression mediated by LINC00467 deficiency.

Conclusions: LINC00467 enhances HNSCC progression by serving as a sponge of miR-299-5p to increase USP48 expression.

Keywords: HNSCC; LINC00467; USP48; miR-299-5p.

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References

REFERENCES

    1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2017. CA Cancer J Clin. 2017;67:7-30.
    1. Kamangar F, Dores GM, Anderson WF. Patterns of cancer incidence, mortality, and prevalence across five continents: defining priorities to reduce cancer disparities in different geographic regions of the world. J Clin Oncol off J am Soc Clin Oncol. 2006;24:2137-2150.
    1. Jou A, Hess J. Epidemiology and molecular biology of head and neck cancer. Oncology Research and Treatment. 2017;40:328-332.
    1. Puram SV, Rocco JW. Molecular aspects of head and neck cancer therapy. Hematol Oncol Clin North am. 2015;29:971-992.
    1. Guo T, Califano JA. Molecular biology and immunology of head and neck cancer. Surg Oncol Clin N am. 2015;24:397-407.

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