Induction of growth arrest by miR-542-3p that targets survivin

Sena Yoon; Young Chul Choi; Suman Lee; Yongsu Jeong; Jaeseung Yoon; Kwanghee Baek

doi:10.1016/j.febslet.2010.08.025

Induction of growth arrest by miR-542-3p that targets survivin

Sena Yoon, Young Chul Choi, Suman Lee, Yongsu Jeong, Jaeseung Yoon, Kwanghee Baek

Research output: Contribution to journal › Article › peer-review

68 Citations (Scopus)

Abstract

Survivin is a protein which functions as a mitotic regulator as well as apoptosis inhibitor. In this study, we show that introduction of synthetic miR-542-3p mimetic reduced both mRNA and protein levels of survivin. In A549 cells, luciferase reporter assay revealed that miR-542-3p targeted predicted binding sites in the 3'-untranslated region (3'-UTR) of survivin. We also demonstrate that ectopic expression of miR-542-3p inhibited cell proliferation by inducing Gap 1 (G1) and Gap 2/Mitosis (G2/M) cell cycle arrest. Collectively, these results suggest that survivin is a direct target of miR-542-3p and growth inhibition by miR-542-3p may have a potential utility as an anti-cancer therapy.

Original language	English
Pages (from-to)	4048-4052
Number of pages	5
Journal	FEBS Letters
Volume	584
Issue number	18
DOIs	https://doi.org/10.1016/j.febslet.2010.08.025
Publication status	Published - Sept 2010

Bibliographical note

Funding Information:
This work was supported by the National Research Foundation of Korea (NRF) Grant funded by the Korea government (MEST) (No. 2009-0075381 ).

Keywords

18S ribosomal RNA
Cell cycle arrest
MiR-542-3p
MicroRNA
Survivin

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.febslet.2010.08.025

Cite this

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title = "Induction of growth arrest by miR-542-3p that targets survivin",

abstract = "Survivin is a protein which functions as a mitotic regulator as well as apoptosis inhibitor. In this study, we show that introduction of synthetic miR-542-3p mimetic reduced both mRNA and protein levels of survivin. In A549 cells, luciferase reporter assay revealed that miR-542-3p targeted predicted binding sites in the 3'-untranslated region (3'-UTR) of survivin. We also demonstrate that ectopic expression of miR-542-3p inhibited cell proliferation by inducing Gap 1 (G1) and Gap 2/Mitosis (G2/M) cell cycle arrest. Collectively, these results suggest that survivin is a direct target of miR-542-3p and growth inhibition by miR-542-3p may have a potential utility as an anti-cancer therapy.",

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author = "Sena Yoon and Choi, {Young Chul} and Suman Lee and Yongsu Jeong and Jaeseung Yoon and Kwanghee Baek",

note = "Funding Information: This work was supported by the National Research Foundation of Korea (NRF) Grant funded by the Korea government (MEST) (No. 2009-0075381 ). ",

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AU - Yoon, Sena

AU - Choi, Young Chul

AU - Lee, Suman

AU - Jeong, Yongsu

AU - Yoon, Jaeseung

AU - Baek, Kwanghee

N1 - Funding Information: This work was supported by the National Research Foundation of Korea (NRF) Grant funded by the Korea government (MEST) (No. 2009-0075381 ).

PY - 2010/9

Y1 - 2010/9

N2 - Survivin is a protein which functions as a mitotic regulator as well as apoptosis inhibitor. In this study, we show that introduction of synthetic miR-542-3p mimetic reduced both mRNA and protein levels of survivin. In A549 cells, luciferase reporter assay revealed that miR-542-3p targeted predicted binding sites in the 3'-untranslated region (3'-UTR) of survivin. We also demonstrate that ectopic expression of miR-542-3p inhibited cell proliferation by inducing Gap 1 (G1) and Gap 2/Mitosis (G2/M) cell cycle arrest. Collectively, these results suggest that survivin is a direct target of miR-542-3p and growth inhibition by miR-542-3p may have a potential utility as an anti-cancer therapy.

AB - Survivin is a protein which functions as a mitotic regulator as well as apoptosis inhibitor. In this study, we show that introduction of synthetic miR-542-3p mimetic reduced both mRNA and protein levels of survivin. In A549 cells, luciferase reporter assay revealed that miR-542-3p targeted predicted binding sites in the 3'-untranslated region (3'-UTR) of survivin. We also demonstrate that ectopic expression of miR-542-3p inhibited cell proliferation by inducing Gap 1 (G1) and Gap 2/Mitosis (G2/M) cell cycle arrest. Collectively, these results suggest that survivin is a direct target of miR-542-3p and growth inhibition by miR-542-3p may have a potential utility as an anti-cancer therapy.

KW - 18S ribosomal RNA

KW - Cell cycle arrest

KW - MiR-542-3p

KW - MicroRNA

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SN - 0014-5793

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IS - 18

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Induction of growth arrest by miR-542-3p that targets survivin

Abstract

Bibliographical note

Keywords

UN SDGs

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