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Antiproliferative potential of miR‐33a in laryngeal cancer Hep‐2 cells via targeting PIM1
Author(s) -
Karatas Omer Faruk
Publication year - 2018
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.25361
Subject(s) - pim1 , oncogene , microrna , cancer research , apoptosis , cancer , western blot , carcinogenesis , downregulation and upregulation , messenger rna , in silico , biology , chemistry , cell cycle , oncology , medicine , microbiology and biotechnology , gene , biochemistry , phosphorylation , serine
Background 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 .