Objective To investigate the effects of ten-eleven translocation (TET1) on the proliferation, metastasis and invasion of breast cancer MDA-MB-231 cells and possible mechanisms.

Methods Breast cancer cell line MDA-MB-231 were stably transfected with recombinant lentiviral expression vector of TET1 and enhanced green fluorescent protein (eGFP). The mRNA and protein expressions of TET1 were detected by Real-time PCR and Western blot. Cell proliferation was detected by CCK-8 assay and flow cytometry was adopted to determine cell cycle distribution. The migration and invasion abilities of cells were detected by wound healing assay and transwell assay. The expression levels of EMT-related protein, such as E-cadherin, N-cadherin, Vimentin and β-catenin, were measured by Western blot and immunofluorescence.

Results A stable overexpression of TET1 cell line was successfully obtained (P=0.030). Cell proliferation, migration and invasion abilities were significantly decreased in MDA-MB-231-TET1 cells(P < 0.001), compared with control group. The overexpression of TET1 suppressed cell proliferation through inducing G₂/M arrest (P=0.002). At the same time, the level of E-cadherin was significantly increased(P < 0.001) and N-cadherin, Vimentin, and β-catenin were decreased(P=0.003, P=0.041, P < 0.001) in MDA-MB-231-TET1 cells. TET1 inhibited the nuclear translocation of β-cantenin and then repressed EMT.

Conclusion The overexpression of TET1 suppresses the proliferation, migration and invasion abilities of MDA-MB-231 cells by inducing EMT through regulating Wnt/β-catenin pathway in vitro.