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miR‐193b promotes cell proliferation by targeting Smad3 in human glioma
Author(s) -
Zhong Qisheng,
Wang Tongli,
Lu Peigang,
Zhang Rongwei,
Zou Jianan,
Yuan Shaoji
Publication year - 2014
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23339
Subject(s) - glioma , downregulation and upregulation , cell growth , microrna , cancer research , transforming growth factor , cell , western blot , biology , microbiology and biotechnology , chemistry , biochemistry , gene
Studies have shown that several miRNAs play important roles in regulating a variety of cellular processes in gliomas. In these reports, upregulation of miR‐193b has been found to be associated with a poor prognosis for glioma, but its functional mechanism in glioma remains unclear. This study investigates the roles of miR‐193b in glioma tumor growth. We first showed that the expression of miR‐193b was elevated in both glioma samples and glioma cells. Furthermore, downregulation of miR‐193b by inhibitors was statistically correlated with a decrease in cell growth and a restored G1 accumulation. Luciferase assay and Western blot analysis revealed that Smad3 is a direct target of miR‐193b. To prove that miR‐193b regulated cell growth through the transforming growth factor‐β (TGF‐β) pathway in glioma cells by regulating Smad3, we tested endogenous targets of the TGF‐β pathway by measuring the accumulation of p21 mRNAs after downregulation of miR‐193b. The results confirmed that induction of p21 was promoted by miR‐193b inhibitors in glioma cells, although this induction disappeared when Smad3 was knocked down with siRNA. Moreover, downregulation of Smad3 mitigates the miR‐193b suppression of glioma proliferation. In conclusion, these results suggest that miR‐193b regulated cell growth in glioma through the TGF‐β pathway by regulating Smad3. Thus, our study indicates that miR‐193b promotes cell proliferation by targeting Smad3 in human glioma, which may serve as a potentially useful target for development of miRNA‐based therapies in the future. © 2014 Wiley Periodicals, Inc.