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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.

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


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.


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

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