Objective: As an essential promoter of papillary thyroid cancer (PTC) metastasis, epithelial-mesenchymal transition (EMT) plays an important role in PTC progression. However, its upstream regulation mechanism is unknown. This study aimed to clarify the specific regulation mechanism of LINC00271 on the EMT of PTC cells. Methods: LINC00271 expression was detected in PTC tissues and PTC cell line TPC-1. The invasive and migratory capabilities of TPC-1 cells were determined by Transwell invasion and wound-healing assays, respectively. The interaction between LINC00271 and trefoil factor 3 (TFF3) was confirmed with RNA pull-down and RNA immunoprecipitation assays. The stability of TFF3 was measured by cycloheximide-chase and ubiquitination assays. Results: LINC00271 was downregulated in both tumor tissue of PTC patients and PTC cell line TPC-1. Its expression inversely correlated with the expression of TFF3. Functionally, LINC00271 overexpression inhibited the EMT of TPC-1 cells and reduced the tumor volumes in xenograft model mice. Further investigation confirmed that LINC00271 bound to TFF3 and suppressed its expression by increasing its ubiquitination level. Moreover, TFF3 overexpression abrogated the inhibitory effect of LINC00271 on the EMT of TPC-1 cells. Conclusion: LINC00271 inhibits the EMT of TPC-1 cells by downregulating TFF3 expression. Keywords: LINC00271, trefoil factor 3, epithelial-mesenchymal transition, papillary thyroid cancer
