Effects of ten-eleven translocation-2 on proliferation and migration as well as invasion of non-small cell lung cancer and its mechanism

  Objective  To discuss the effect of ten-eleven tanslocation-2 (TET2) on the proliferation, migration and invasion of non-small cell lung cancer (NSCLC) and its mechanism.

  Methods  Online databases were used to detect the correlation between TET2 expression and prognosis of NSCLC patients; quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were performed to detect the expression of TET2 bronchial epithelial cells and non-small cell lung cancer lines; after transient transfection with si-TET2, cell proliferation were detected by CCK8 and clonogenic assay; Transwell assay was used to detect cell migration and invasion; cell cycle changes were detected by flow cytometry; epithelial-mesenchymal transition (EMT) markers and protein levels of N-cadherin, E-cadherin Vimentin and Cyclin D1 were detected by Western blot.

  Results  Patients with high TET2 expression had poor overall survival. Compared with normal human lung epithelial cells, TET2 is highly expressed in NSCLC cell lines. TET2 knockdown significantly inhibited the proliferation, migration and invasion of A549 and H1299 cells (P < 0.001), and blocked the cell cycle in the G₀/G₁ phase. Western blot results showed that the protein expressions of N-cadherin, Vimentin and Cyclin D1 were significantly down-regulated, while the expression of E-cadherin was significantly up-regulated (P < 0.05, P < 0.01 or P < 0.001).

  Conclusion  TET2 may promote the proliferation, migration and invasion of NSCLC by affecting the cell cycle and key proteins of EMT.