miR-181a Targets GATA6 to Inhibit the Progression of Human Laryngeal Squamous Cell Carcinoma

Abstract

Aim: We sought to determine the function of miR-181a/GATA6 pathway in the progression of laryngeal squamous cell carcinoma (LSCC). Materials & methods: The expression of miR-181a and GATA6 were detected using quantitative real-time-PCR and western blotting in 127 LSCC samples and 32 corresponding control mucosa tissues. Cell death, migration and apoptosis were measured in Hep-2 cells using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), Transwell migration assay and apoptosis assay, respectively. The prognosis was determined by the follow-up, univariate analysis and multivariate analysis. Results: We observed decreased miR-181a levels and increased GATA6 expression in LSCC samples compared with control mucosa tissues. Transfection of miR-181a decreased GATA6 expression, suppressed migration and promoted apoptosis in Hep-2 cells. Furthermore, silencing GATA6 suppressed cell migration and promoted apoptosis in Hep-2 cells. Notably, patients with high miR-181a levels had a longer life span. Conclusion: MiR-181a inhibits LSCC progression via suppressing GATA6 expression. MiR-181a is an independent prognostic factor in LSCC patients.

Keywords::

• cervical metastasis
• GATA6
• laryngeal cancer
• LSCC
• miR-181a
• prognosis
• tumor progression

Supplementary data

To view the supplementary data that accompany this paper, please visit the journal website at: www.tandfonline.com/doi/suppl/10.2217/fon-2018-0064

Acknowledgements

The manuscript was revised by Dr QJ Zhang of University of Iowa, IA, USA.

Financial & competing interests disclosure

This work is supported by National Natural Science Foundation of China (no. 81302364). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work is supported by National Natural Science Foundation of China (no. 81302364). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.