Retracted: MicroRNA‐150‐5p affects cell proliferation, apoptosis, and EMT by regulation of the BRAFV600E mutation in papillary thyroid cancer cells

Abstract

Papillary thyroid cancer (PTC) is the most common endocrine malignancy. Studies have confirmed an association between microRNA (miRNA) and the BRAFV600E mutation in various cellular biological processes of PTC. This study aimed to clarify the potential relationship between miR-150-5p and the BRAFV600E mutation in PTC. Human PTC cell lines B-CPAP and TPC-1 were transfected with the miR-150-5p mimic, an inhibitor, and the corresponding controls. Then, cell proliferation, viability, and apoptosis were detected by bromodeoxyuridine, trypan blue exclusion, and flow cytometry assays. The expressions of the main factors of cell cycle, epithelial mesenchymal transition (EMT), and DNA mismatch repair were examined by Western blot analysis and a real-time quantitative polymerase chain reaction. Additionally, pc-BRAFV600E was transfected into B-CPAP and TPC-1 cells to determine the relationship between miR-150-5p and BRAFV600E . In addition, the methyl ethyl ketone (MEK)/extracellular signal-regulated kinase (ERK) signal pathway was examined using Western blot analysis. Overexpression of miR-150-5p promoted cell proliferation and viability, inhibited apoptosis, and upregulated cell cycle factor expressions at 50 passages of B-CPAP and TPC-1 cells after transfection. Overexpression of miR-150-5p led to an obvious decrease in E-cadherin expression, but enhanced N-cadherin, Slug and Vimentin, ZEB1, and Snail expression. Moreover, overexpression of miR-150-5p markedly suppressed POLD3, MSH2, and MSH3 expression. Furthermore, BRAFV600E overexpression increased the expression level of miR-150-5p in TPC cells, and overexpression of telomerase reverse transcriptase further enhanced the promoting effect of BRAFV600E on miR-150-5p expression in B-CPAP and TPC-1 cells. Finally, BRAFV600E overexpression activated the MEK/ERK signal pathway in B-CPAP and TPC-1 cells. These data indicated that miR-150-5p promoted cell proliferation, suppressed apoptosis, and accelerated the EMT process by regulation of the BRAFV600E mutation. Our findings will help elucidate the pathogenesis of PTC and identify biomarkers.