LINC00511 influences cellular proliferation through cyclin-dependent kinases in papillary thyroid carcinoma

Background: Proverbially, the incidence rate of papillary thyroid carcinoma (PTC) has increased year by year. Many long noncoding RNAs (lncRNAs) have been discovered having a relationship with tumor genesis tightly recently. Thanks to the previous researches, we found long intergenic noncoding RNA 00511 (LINC00511) is overexpressed and acts as an oncogene in non-small-cell lung cancer and breast cancer. However, the biological role and function of LINC00511 are still unclear in PTC. Methods: We got the expression of LINC00511 in PTC tissues and matched adjacent tissues, as well the cell lines (B-CPAP, KTC-1, and KTC-1) by way of quantitative real-time polymerase chain reaction (qRT-PCR). In vitro, we knocked down the LINC00511 with small interfering RNA in PTC cell lines and demonstrated the function of LINC00511 by Cell Counting Kit-8, cell colony formation, Transwell migration, Transwell invasion, apoptosis assays, and cell cycle assays. Then, we discovered several downstream proteins of LINC00511 using Western blotting. Results: We proved that LINC00511's expression in PTC tissues and cell lines is higher than the control. LINC00511 promoted cellular proliferation, migration, invasion, G1/S transition and reduced apoptosis in vitro experiment. Knocked-down of LINC00511 resulted in the reduction of histone methyltransferase enhancer of zeste homolog 2 (EZH2), cyclin-dependent kinase 2 (CDK2) and cyclin-dependent kinase 4 (CDK4). Conclusions: Our results certified the role and function of LINC00511 in PTC, and it could become a novel tumor therapeutic target.