miR-509 inhibits cancer stemness properties in oral carcinomas via directly targeting PlK1

Background/purpose: Oral cancer is one of the common cancers worldwide. Emerging evidence has indicated that microRNAs (non-coding RNA molecules of approximately 22 nucleotides in length) are implicated in the regulation of cancer stemness. However, the functional role of microRNA-509 (miR-509) in the characteristics of oral cancer stem cells (CSCs) has not been unraveled. Materials and methods: The expression level of miR-509 in ALDH1(+) and sphere oral CSCs was examined by qRT-PCR. The aldehyde dehydrogenase 1 (ALDH1) activity and CD44 expression were assessed using flow cytometry. Self-renewal, transwell migration, and colony formation assays were conducted to measure the CSC phenotypes. Besides, a luciferase reporter assay was used to confirm the direct interaction between miR-509 and its target polo-like kinase 1 (plk1). Results: We showed the expression of miR- 509 was downregulated in the CSCs derived from oral cancer cells (SAS), and upregulation of miR-509 diminished the several CSCs features, including ALDH1 activity, self-renewal capacity, CD44 expression, migration, and colonyforming abilities. Moreover, the result from the luciferase reporter assay validated the direct binding of miR-509 to plk1. Conclusion: Our results suggest that the miR-509/plk1 axis may mediate the cancer stemness in oral cancer, and targeting this axis may attenuate the progression of oral cancer. (C) 2021 Association for Dental Sciences of the Republic of China. Publishing services by Elsevier B.V.

Automated summary

The study identified that miR-509 expression is downregulated in oral cancer stem cells and upregulation of miR-509 can attenuate various characteristics of CSCs. A luciferase reporter assay confirmed the direct binding between miR-509 and plk1, suggesting the potential role of miR-509/plk1 axis in mediating cancer stemness in oral cancer and providing a potential therapeutic target.