MiR-365a-3p suppresses proliferation and invasion of Hep-2 cells through targeting ten-eleven translocation 1 (TET1)

miRNAs are among the most important factors that regulate gene expression. Bioinformatic analysis supports our prediction that miR-365a-3p affects tumor biological processes through TET1, so TET1 interference and miR-365a-3p inhibitor constructs were generated. qRT-PCR verified the expression level of miR-365a-3p and TET1 in Hep-2 and BESB-2B cells and qRT-PCR and Western blot were used to confirm the TET1 expression level in Hep-2 and miR-365a-3p inhibitor cells. Cell proliferation, cell cycle progression and cell invasion were further studied to identify the relationship between TET1 and miR-365a-3p. Luciferase reporter gene assays were used to find the binding site of miR-365a-3p in the 3'-UTR (3'-untranslated region) of the TET1 mRNA. TET1 was weakly expressed in Hep-2 cells and highly expressed in BESB-2B cells, while miR-143-3p and miR-365a-3p were highly expressed in Hep-2 cells and lowly expressed in BESB-2B cells. Inhibiting miR-365a-3p could up-regulate the expression of TET1 and the negative effects of miR-365a-3p on cell proliferation, cell cycle progression and cell invasion could be abolished by TET1 interference. The miR-365a-3p binding site is in the 3'-UTR of the TET1 mRNA. TET1 is one of miR-365a-3p's targets and miR-365a-3p regulates the biological behavior of laryngeal cancer by down-regulating TET1.