Abstract
Emerging evidence has shown that long noncoding RNA (lncRNA) plays an important role in various types of malignant cancer. Small nucleolar RNA host gene 12 (SNHG12) was found to be upregulated and to act as an oncogene in several cancers. However, the function and regulatory mechanism of SNHG12 remain unclear in papillary thyroid carcinoma (PTC). In this study, SNHG12 was found to be increased in PTC tissues and cell lines using quantitative real-time PCR. Knockdown of SNHG12 significantly inhibited PTC cell proliferation, migration and invasion and induced apoptosis in vitro. Mechanistic investigations revealed that SNHG12 functions as a competing endogenous RNA (ceRNA) to sponge miR-16-5p, which was downregulated in PTC tissues. In addition, rescue assays further confirmed that SNHG12 contributed to the progression of PTC through regulating miR-16-5p expression. These results indicated that SNHG12 might contribute to tumor progression in PTC by acting as a ceRNA to sponge miR-16-5p.
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