The long noncoding RNA myocardial infarction associated transcript (MIAT) was reported to be involved in the progression of multiple cancers. However, the exact roles and molecular mechanisms of MIAT in papillary thyroid cancer (PTC) progression are still unknown. We examined the expression levels of lncRNA MIAT in 50 paired PTC tissue specimens and four PTC cell lines by real time quantitative PCR (qRT-PCR). Cell counting kit 8, colony formation, wound healing and transwell assays were performed to examine the effect of MIAT on proliferation, colony formation, migration and invasion. Tumor xenograft models were created to detect the role of MIAT in vivo tumorigenesis. The target relationships were predicted by miRcode algorithm, and confirmed by dual luciferase reporter gene assay and qRT-PCR. We found that MIAT was up-regulated in PTC tissues and cell lines. High MIAT expression was positively associated with advanced tumor-node-metastasis (TNM) stage and lymph node metastasis. Functional assays showed that knockdown of MIAT in PTC cells significantly inhibited cell proliferation, colony formation, migration and invasion in vitro, as well as impaired tumor growth in vivo. Luciferase assays further confirmed that miR-212 interacts with MIAT. Additionally, the negatively correlation of miR-212 with MIAT was verified in patients' samples. Repression of miR-212 partly abrogated the inhibitory effects of MIAT knockdown on PTC cells. Taken together, these results indicated that MIAT might be an oncogenic lncRNA that promoted PTC progression, and might be a potential therapeutic target for PTC.