Sugang Ma1, Wei Jia2, Shiyu Ni3. 1. Breast Surgery, The Sixth People's Hospital of Ji'nan, 250200, China. 2. Department Two of General Surgery, Yulin First Hospital of Shanxi, 718000, China. 3. Department of General Surgery, Longnan Hospital of Daqing, Heilongjiang, 163453, China. Electronic address: nsy123good@sina.com.
Abstract
BACKGROUND: Increasing evidence has emphasized the important roles of differentially expressed miRNAs in papillary thyroid cancer (PTC) development. miR-199a-5p was previously documented to be downregulated in PTCs compared with normal thyroids. However, the role of miR-199a-5p in the progression of PTC and the underlying mechanism remain to be further addressed. METHODS: miR-199a-5p and snail family zinc finger 1 (SNAI1) mRNA expressions in PTC tissues and cells were detected by qRT-PCR. The effects of miR-199a-5p and SNAI1 on cell migration, invasion and epithelial-mesenchymal transition (EMT) were evaluated by cell migration and invasion assays, and western blot, respectively. The relationship between miR-199a-5p and SNAI1 was investigated by luciferase reporter assay and western blot. Xenograft tumor assay was performed to verify the role of miR-199a-5p and molecular mechanism in PTC. RESULTS: miR-199a-5p expression was significantly downregulated and SNAI1 was markedly upregulated in PTC tissues and cells. miR-199a-5p overexpression and SNAI1 knockdown suppressed the progression of PTC cells in vitro, as evidenced by the reduced cell migration, invasion and EMT. Of note, SNAI1 was identified as a target of miR-199a-5p and miR-199a-5p suppressed SNAI1 expression in PTC cells. Xenograft tumor assay proved that miR-199a-5p overexpression suppressed tumor growth in PTC in vivo by downregulating SNAI1. CONCLUSION: miR-199a-5p inhibited the progression of PTC by downregulating SNAI1, offering new insight into the molecular mechanism underlying PTC progression.
BACKGROUND: Increasing evidence has emphasized the important roles of differentially expressed miRNAs in papillary thyroid cancer (PTC) development. miR-199a-5p was previously documented to be downregulated in PTCs compared with normal thyroids. However, the role of miR-199a-5p in the progression of PTC and the underlying mechanism remain to be further addressed. METHODS:miR-199a-5p and snail family zinc finger 1 (SNAI1) mRNA expressions in PTC tissues and cells were detected by qRT-PCR. The effects of miR-199a-5p and SNAI1 on cell migration, invasion and epithelial-mesenchymal transition (EMT) were evaluated by cell migration and invasion assays, and western blot, respectively. The relationship between miR-199a-5p and SNAI1 was investigated by luciferase reporter assay and western blot. Xenograft tumor assay was performed to verify the role of miR-199a-5p and molecular mechanism in PTC. RESULTS:miR-199a-5p expression was significantly downregulated and SNAI1 was markedly upregulated in PTC tissues and cells. miR-199a-5p overexpression and SNAI1 knockdown suppressed the progression of PTC cells in vitro, as evidenced by the reduced cell migration, invasion and EMT. Of note, SNAI1 was identified as a target of miR-199a-5p and miR-199a-5p suppressed SNAI1 expression in PTC cells. Xenograft tumor assay proved that miR-199a-5p overexpression suppressed tumor growth in PTC in vivo by downregulating SNAI1. CONCLUSION:miR-199a-5p inhibited the progression of PTC by downregulating SNAI1, offering new insight into the molecular mechanism underlying PTC progression.