Antiproliferative potential of miR-33a in laryngeal cancer Hep-2 cells via targeting PIM1.

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. 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. 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. Mir-33a was demonstrated to act as a tumor suppressor in larnygeal cancer via directly targeting the 3' untranslated region of PIM1.

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Long non-coding RNA LINC01003 suppresses the development of multiple myeloma by targeting miR-33a-5p/PIM1 axis.

Numerous long non-coding RNAs (lncRNAs) are reported to affect the progression of multiple myeloma (MM). This study is aimed to explore the role and downstream mechanism of lncRNA LINC01003 in MM. Xenograft tumor assay was used to assess the function of LINC01003 in MM in vivo. The mRNA expression levels of LINC01003, miR-33a-5p, and PIM1 were determined by quantitative real-time polymerase chain reaction. Cell viability was examined by MTT assay. Relative protein levels of apoptosis-related factors (Bcl-2 and Bax) and proviral integration site of the Moloney leukemia virus kinase 1 (PIM1) were detected via western blot. Adhesion-related proteins were measured by Enzyme-linked immunosorbent assay was used to determine the levels of adhesion-related proteins. Besides, the target relation among LINC01003, miR-33a-5p and PIM1 was tested via dual-luciferase reporter assay. Low expression of LINC01003 was observed in MM cell lines and peripheral blood samples of MM patients. Both LINC01003 up-regulation and miR-33a-5p down-regulation repressed cell viability and adhesion, and promoted apoptosis of MM cells. Moreover, LINC01003 suppressed the growth of xenograft tumor in mice. We then identified miR-33a-5p as a downstream target of LINC01003, and confirmed that PIM1 was a direct target gene of miR-33a-5p. Both high expression of miR-33a-5p and low expression of PIM1 reversed the suppressive effects of LINC01003 overexpression on cell adhesion and viability, and the promoting effect on apoptosis in MM cells. LINC01003 functioned as a sponge of miR-33a-5p to inhibit the development MM by regulating PIM1 expression.

Wu L ，Xia L ，Chen X ，Ruan M ，Li L ，Xia R ... -  《-》

The proto-oncogene Pim-1 is a target of miR-33a.

Thomas M ，Lange-Grünweller K ，Weirauch U ，Gutsch D ，Aigner A ，Grünweller A ，Hartmann RK ... -  《-》

Biological function and mechanism of miR-33a in prostate cancer survival and metastasis: via downregulating Engrailed-2.

Li Q ，Lu S ，Li X ，Hou G ，Yan L ，Zhang W ，Qiao B ... -  《-》

Upregulation of miR-129-5p affects laryngeal cancer cell proliferation, invasiveness, and migration by affecting STAT3 expression.

Shen N ，Huang X ，Li J 《-》