Downregulation of PRMT1 promotes the senescence and migration of a non-MYCN amplified neuroblastoma SK-N-SH cells

doi:10.1038/s41598-018-38394-6

中山醫學大學機構典藏 CSMUIR > 醫學科技學院 > 生物醫學科學學系暨碩士班 > 期刊論文 > Item 310902500/19896

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/19896

Title:	Downregulation of PRMT1 promotes the senescence and migration of a non-MYCN amplified neuroblastoma SK-N-SH cells
Authors:	Lee, Y.-J Chang, W.-W Chang, C.-P Liu, T.-Y Chuang, C.-Y Li, C.
Contributors:	中山醫學大學生物醫學科學學系（所）
Date:	2019-03
Issue Date:	2019-03-12T03:05:21Z (UTC)
ISSN:	20452322
Abstract:	Protein arginine methyltransferase 1 (PRMT1) catalyzing the formation of asymmetric dimethylarginines has been implicated in cancer development, metastasis, and prognosis. In this study, we investigated the effects of low PRMT1 levels on a non-MYCN amplified neuroblastoma SK-N-SH cell line. Stable PRMT1-knockdown (PRMT1-KD) cells showed reduced growth rates and cell cycle arrest at G 2 /M. They also exhibited senescent phenotypes and increased p53 expression. p21 and PAI-1, which are two p53 downstream targets critical for senescence, were significantly induced in SK-N-SH cells subjected to either PRMT1-KD or inhibitor treatment. The induction was suppressed by a p53 inhibitor and marginal in a p53-null SK-N-AS cell line, suggesting dependence on p53. In general, the DNA damage and ROS levels of the PRMT1-KD SK-N-SH cells were slightly increased. Their migration activity also increased with the induction of PAI-1. Thus, PRMT1 downregulation released the repression of cellular senescence and migration activity in SK-N-SH cells. These results might partially explain the poor prognostic outcome of low PRMT1 in a non-MYCN-amplified cohort and indicate the multifaceted complexity of PRMT1 as a biological regulator of neuroblastoma. © 2019, The Author(s).
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/19896
Relation:	Scientific Reports Volume 9, Issue 1, 1 December 2019
Appears in Collections:	[生物醫學科學學系暨碩士班] 期刊論文

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