Long noncoding RNA SNHG6 promotes papillary thyroid cancer cells proliferation via regulating miR-186/CDK6 axis

Papillary thyroid cancer (PTC) is a common endocrine malignancy, and its incidence rate has been increasing in recent years. Long noncoding RNAs (lncRNAs) participate in cell biological processes through a variety of regulatory ways, and play an essential role in tumor development.

This study explored the expression of lncRNA small nucleolar RNA host gene 6 (SNHG6) in PTC by bioinformatics analysis, and quantitative real-time PCR (qRT-PCR). Cell counting kit-8 (CCK-8) assay, colony formation assay, and 5-ethynyl-2'-deoxyuridine (EdU) assay were used to study the effect of SNHG6 on the proliferation of PTC cells. Luciferase reporter gene assay and western blot were used to study the mechanism.

SNHG6 was highly expressed in PTC tissue samples and cell lines. In vitro, overexpression of SNHG6 promoted the proliferation of PTC cells, while silencing SNHG6 inhibited the proliferation of PTC cells. miR-186 is the downstream target of SNHG6. SNHG6 regulates the proliferation of PTC cells through miR-186. In addition, CDK6 is the target gene of miR-186, which can inhibit the expression of CDK6 protein. SNHG6 can promote the expression of CDK6 by regulating miR-186.

SNHG6 is highly expressed in PTC and can promote the proliferation of PTC cells by regulating the miR-186/CDK6 axis, which is expected to become a potential therapeutic target for PTC.