Laryngeal cancer is a frequent cause of cancer-associated mortality worldwide with an overall poor prognosis along with high mortality rates. Therefore, comprehensive investigation of underlying molecular mechanisms of laryngeal carcinogenesis remains an important problem.Methods
In this study, proliferative and apoptotic features of Hep-2 cells overexpressing microRNA-33a (miR-33a) were evaluated and in silico analysis along with literature search was used to find putative targets of miR-33a. The potential of PIM1 (pim-1 oncogene) as a direct target of miR-33a was tested using quantitative real-time polymerase chain reaction, Western blot, and luciferase assay.Results
Induced miR-33a expression significantly inhibited proliferation through inducing apoptosis of Hep-2 cells. Further in vitro tests showed downregulation of PIM1 in messenger ribonucleic acid (mRNA) and protein level upon miR-33a overexpression and confirmed PIM1 as a direct target of miR-33a.Conclusions
Mir-33a was demonstrated to act as a tumor suppressor in larnygeal cancer via directly targeting the 3′ untranslated region of PIM1.