Retracted: Expression Of Mir-106a In Thyroid Carcinoma And Its Effect On The Proliferation And Invasion Of Thyroid Cancer Cell Line Sw579 By Targeting Cdh1(Retracted Article. See Vol.10, Pg.8097, 2017)

Background: To investigate the expression of miR-106a in thyroid cancer and its effect on the proliferation, metastasis and invasion of thyroid cancer by targeting epithelial cadherin 1 (CDH1). Methods: Real-time quantitative reverse transcription polymer chain reaction (RT-qPCR) was used to quantify the expression of miR-106a in human papillary thyroid carcinoma (PTC) tissues and adjacent normal tissues. miR-106a inhibitor and miR-106a NC were transfected into human thyroid cancer cell line SW579 using Lipofectamine (TM) 2000 to assess their effect on cell viability and apoptosis using the MTT method and flow cytometry after Annexin V/PI double staining. The invasion ability was assayed with the Transwell method. The expression of CDH1 at protein and mRNA levels was analyzed using Western blot and RT-qPCR and confirmed using dual luciferase reporter assay. Finally, CDH1 low expression vector (siRNA-CDH1) were transfected into SW579 cells together with miR-106a inhibitor. The transfected cells were examined for apoptosis and invasion ability, as well as the expression of Snail, E-cadherin, Vimentin, retinal glioblastoma gene (Rb1) and transcriptional factor E2F1. Results: The expression of miR-106a in PTC tissues was higher than that in adjacent normal tissues (P<0.01). miR-106a inhibitor significantly reduced the viability and invasion ability of SW579 cells (P<0.01), increased apoptosis (P<0.01), and down regulated the expression of CDH1 at protein and mRNA levels (P<0.01). The luciferase reporter assay confirmed that CDH1 was a downstream target gene of miR-106a. Co-transfection of SW579 cells with SiRNA-CDH1 and miR-106a inhibitor significantly offset the inhibitory effect of the miR-106a inhibitor on the proliferation and invasion of SW579 cells (P<0.01), and the induction of apoptosis (P<0.01). These effects may result from up-regulated expression of E2F1, Snail and Vimentin (P<0.01), and down-regulated expression of Rb1 and E-cadherin (P<0.01). Conclusion: miR-106a is highly expressed in PTC. Down-regulation of its expression results in targeted up-regulation of CDH1, thus inhibiting the proliferation and invasion ability of SW579 cells. This process is likely mediated by up-regulation of Rb1 and E-cadherin expression and down-regulation of Snail and E2F1 and Vimentin expression.