Thyroid carcinoma is a common malignant tumor of endocrine system and head and neck. Recurrence, metastasis and high malignant expression after routine treatment are serious clinical problems, so it is of great significance to explore its mechanism and find action targets. Epithelial–mesenchymal transition (EMT) is associated with tumor malignancy and invasion. One key change in tumour EMT is low expression of E-cadherin. Therefore, this article reviews the expression of E-cadherin in thyroid cancers (TC), discuss the potential mechanisms involved, and outline opportunities to exploit E-cadherin on regulating the occurrence of EMT as a critical factor in cancer therapeutics.

We aimed to explore the mechanism underlying the role of bone marrow mesenchymal stem cells (BMSCs) in the invasion of papillary thyroid cancer (PTC) cells. BMSCs were co-cultured with PTC cells WRO or normal thyroid follicular epithelial cells T3TD followed by analysis of cell migration and proliferation by Transwell assay and MTT assay. Cells were transfected with shRNA or overexpression of PTBP1, followed by measuring cell proliferation and invasion and PTBP1 expression by RT-qPCR and Western blot. Co-cultivation with MSC promoted the malignant transformation of WRO, inhibited the RNA-binding protein PTBP1 and activation of GS3Kβ/Akt. In addition, silencing of PTBP1 accelerated cell invason and induced overexpression of EMT proteins, while overexpression of PTBP1 inhibited cell proliferation and migration. In conclusion, BMSCs might promote PTC invasion and metastasis by inhibiting PTBP1 expression, providing a novel insight into the treatment of PTC.