Abstract
miR-212 as a tumor suppressor has been reported to be downregulated in multiple cancer cells lines and tumor tissues. However, its role in thyroid cancer has nor been investigated. Therefore, the present study aimed to investigate the role of miR-212 in human thyroid cancer and the underlying mechanisms. In the present study, we demonstrated that miR-212 expression was significantly decreased in thyroid cancer specimens and cell lines compared with adjacent normal tissues and normal thyroid cell lines. In addition, we demonstrated that miR-212 downrwegulation in thyroid cancer tissues was negatively associated with lymph node metastasis and advanced clinical stage. Functionally, ectopic expression of miR-212 by transfection with miR-212 mimic significantly inhibited proliferation, colony formation, migration and invasion in TPC-1 cells. In addition, Sirtuin 1 (SIRT1) was identified as a direct target of miR-212 and its expression was inversely correlated with miR-212 expression in thyroid cancer tissues. Overexpression of SIRT1 could effectively rescue miR-212 mimic-induced suppression of cell proliferation, migration and invasion in TPC-1 cells. Invivo, miR-212 overexpression significantly inhibited tumor growth in a nude mice model. In light of these findings, miR-212 may function as a tumor suppressor in thyroid cancer by targeting SIRT1.
Highlights
Abstract. miR-212 as a tumor suppressor has been reported to be downregulated in multiple cancer cells lines and tumor
We found that miR-212 was downregulated in thyroid cancer cell lines compared with the human thyroid epithelial cell line (Fig. 1D)
TPC-1 cell line exhibited the lowest levels of miR-212 expression and was used for subsequent studies (Fig. 1D). These results indicated that low miR-212 may be associated with thyroid cancer progression
Summary
Abstract. miR-212 as a tumor suppressor has been reported to be downregulated in multiple cancer cells lines and tumor. CCK-8 assays demonstrated that miR-212 overexpression significantly inhibited thyroid cancer cell proliferation (Fig. 2B). That the expression levels of miR-212 in advanced clinical stage (III‐IV) were significantly downregulated compared with those SIRT1 is a direct target of miR-212 in thyroid cancer cells.
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