Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation

Abstract Background: SET domain bifurcated 1 (SETDB1) has been widely considered as an oncogene playing a critical role in many human cancers, including breast cancer. Nevertheless, the molecular mechanism by which SETDB1 regulates breast cancer tumorigenesis is still unknown. Methods: qRT-PCR ass...

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Autores principales:	Wu,Milu, Fan,Baohua, Guo,Qijing, Li,Yan, Chen,Rong, Lv,Nannan, Diao,Yinzhuo, Luo,Yushuang
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2018
Materias:	SET domain bifurcated 1 miR-381-3p Breast cancer Proliferation Cell cycle progression Migration
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100232
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spelling	oai:scielo:S0716-976020180001002322018-12-05Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulationWu,MiluFan,BaohuaGuo,QijingLi,YanChen,RongLv,NannanDiao,YinzhuoLuo,Yushuang SET domain bifurcated 1 miR-381-3p Breast cancer Proliferation Cell cycle progression Migration Abstract Background: SET domain bifurcated 1 (SETDB1) has been widely considered as an oncogene playing a critical role in many human cancers, including breast cancer. Nevertheless, the molecular mechanism by which SETDB1 regulates breast cancer tumorigenesis is still unknown. Methods: qRT-PCR assay or western blot analysis was performed to assess the expression level of SETDB1 mRNA or protein, respectively. siSETDB1, pCMV6-XL5-SETDB1, miR-381-3p mimic, or miR-381-3p inhibitor was transfected into cells to regulate the expression of SETDB1 or miR-381-3p. MiRNA directly interacted with SETDB1 was verified by luciferase reporter assay and RNA immunoprecipitation. CCK-8 assay, colony formation assay, flow cytometric analysis, and transwell assay were used to detect the abilities of cell proliferation, cell cycle progression and migration, respectively. Animal model of xenograft tumor was used to observe the regulatory effect of SETDB1 on tumor growth in vivo. Results: We verified that SETDB1 mRNA level was upregulated in breast cancer tissues and cell lines, and SETDB1 depletion led to a suppression of cell proliferation, cell cycle progression and migration in vitro, as well as tumor growth in vivo. SETDB1 was verified to be a target of miR-381-3p. Moreover, miR-381-3p overexpression suppressed cell proliferation, cell cycle progression and migration, whereas SETDB1 abated miR-381-3p-mediated regulatory function on breast cancer cells. Conclusions: This study revealed that SETDB1 knockdown might suppress breast cancer progression at least partly by miR-381-3p-related regulation, providing a novel prospect in breast cancer therapy.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.51 20182018-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100232en10.1186/s40659-018-0189-0
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	SET domain bifurcated 1 miR-381-3p Breast cancer Proliferation Cell cycle progression Migration
spellingShingle	SET domain bifurcated 1 miR-381-3p Breast cancer Proliferation Cell cycle progression Migration Wu,Milu Fan,Baohua Guo,Qijing Li,Yan Chen,Rong Lv,Nannan Diao,Yinzhuo Luo,Yushuang Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation
description	Abstract Background: SET domain bifurcated 1 (SETDB1) has been widely considered as an oncogene playing a critical role in many human cancers, including breast cancer. Nevertheless, the molecular mechanism by which SETDB1 regulates breast cancer tumorigenesis is still unknown. Methods: qRT-PCR assay or western blot analysis was performed to assess the expression level of SETDB1 mRNA or protein, respectively. siSETDB1, pCMV6-XL5-SETDB1, miR-381-3p mimic, or miR-381-3p inhibitor was transfected into cells to regulate the expression of SETDB1 or miR-381-3p. MiRNA directly interacted with SETDB1 was verified by luciferase reporter assay and RNA immunoprecipitation. CCK-8 assay, colony formation assay, flow cytometric analysis, and transwell assay were used to detect the abilities of cell proliferation, cell cycle progression and migration, respectively. Animal model of xenograft tumor was used to observe the regulatory effect of SETDB1 on tumor growth in vivo. Results: We verified that SETDB1 mRNA level was upregulated in breast cancer tissues and cell lines, and SETDB1 depletion led to a suppression of cell proliferation, cell cycle progression and migration in vitro, as well as tumor growth in vivo. SETDB1 was verified to be a target of miR-381-3p. Moreover, miR-381-3p overexpression suppressed cell proliferation, cell cycle progression and migration, whereas SETDB1 abated miR-381-3p-mediated regulatory function on breast cancer cells. Conclusions: This study revealed that SETDB1 knockdown might suppress breast cancer progression at least partly by miR-381-3p-related regulation, providing a novel prospect in breast cancer therapy.
author	Wu,Milu Fan,Baohua Guo,Qijing Li,Yan Chen,Rong Lv,Nannan Diao,Yinzhuo Luo,Yushuang
author_facet	Wu,Milu Fan,Baohua Guo,Qijing Li,Yan Chen,Rong Lv,Nannan Diao,Yinzhuo Luo,Yushuang
author_sort	Wu,Milu
title	Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation
title_short	Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation
title_full	Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation
title_fullStr	Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation
title_full_unstemmed	Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation
title_sort	knockdown of setdb1 inhibits breast cancer progression by mir-381-3p-related regulation
publisher	Sociedad de Biología de Chile
publishDate	2018
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602018000100232
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_version_	1718441576053604352

Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation

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