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J Cell Mol Med. 2019 Apr;23(4):2813-2821. doi: 10.1111/jcmm.14189. Epub 2019 Feb 7.

MicroRNA-1258, regulated by c-Myb, inhibits growth and epithelial-to-mesenchymal transition phenotype via targeting SP1 in oral squamous cell carcinoma.

Author information

1
Department of Medical Oncology, Guangdong General Hospital and Guangdong Academy of Medical Sciences, Guangzhou, China.
2
Department of Oral and Maxillofacial Surgery, Guangdong General Hospital and Guangdong Academy of Medical Sciences, Guangzhou, China.
3
Department of Operation Room, Affiliated Cancer Hospital of Guangzhou Medical University, Guangzhou, China.
4
Department of Thyroid and Breast Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.

Abstract

The biological function and underlying mechanism of miR-1258 has seldom been investigated in cancer progression, including in oral squamous cell carcinoma (OSCC). In the current study, we revealed that the expression level of miR-1258 was significantly down-regulated in OSCC tissues and cell lines. Restoration of miR-1258 decreased OSCC cell growth and invasion. The luciferase and Western blot assays revealed that SP1 protein was a downstream target of miR-1258. Overexpression of SP1 dismissed miR-1258's effect on cell growth and invasion. We also revealed that c-Myb inhibited miR-1258 by directly binding at its promoter. In addition, miR-1258 inhibited PI3K/AKT and ERK signalling pathway activity. Taken together, these findings demonstrated that miR-1258 may function as a tumour-suppressive micorRNA in OSCC and suggested that miR-1258 may be a potential therapeutic target for OSCC patients.

KEYWORDS:

SP1; c-Myb; miR-1258; oral squamous cell carcinoma

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