The long noncoding RNA of RMRP is downregulated by PERK, which induces apoptosis in hepatocellular carcinoma cells

Abstract Endoplasmic reticulum (ER) stress plays an important role in hepatocyte degeneration, especially in patients with chronic liver injury. Protein kinase R-like endoplasmic reticulum kinase (PERK) is a key molecule in ER stress. PERK may contribute to apoptotic cell death in HCC, however the d...

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Autores principales:	Atsushi Yukimoto, Takao Watanabe, Kotaro Sunago, Yoshiko Nakamura, Takaaki Tanaka, Yohei Koizumi, Osamu Yoshida, Yoshio Tokumoto, Masashi Hirooka, Masanori Abe, Yoichi Hiasa
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c81affd535aa44499e9b9374cdcaecf6
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spelling	oai:doaj.org-article:c81affd535aa44499e9b9374cdcaecf62021-12-02T14:27:59ZThe long noncoding RNA of RMRP is downregulated by PERK, which induces apoptosis in hepatocellular carcinoma cells10.1038/s41598-021-86592-62045-2322https://doaj.org/article/c81affd535aa44499e9b9374cdcaecf62021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-86592-6https://doaj.org/toc/2045-2322Abstract Endoplasmic reticulum (ER) stress plays an important role in hepatocyte degeneration, especially in patients with chronic liver injury. Protein kinase R-like endoplasmic reticulum kinase (PERK) is a key molecule in ER stress. PERK may contribute to apoptotic cell death in HCC, however the details of the mechanism are not clear. In this study, we identified PERK-associated molecules using transcriptome analysis. We modulated PERK expression using a plasmid, tunicamycin and siRNA against PERK, and then confirmed the target gene expression with real-time PCR and Northern blotting. We further analyzed the apoptotic function. Transcriptome analysis revealed that expression of the RNA component of mitochondrial RNA processing endoribonuclease (RMRP), which is a long noncoding RNA, was strongly correlated with the function of PERK. The expression of RMRP was correlated with the expression of PERK in experiments with the siRNA and PERK plasmid in both HCC cell lines and human HCC tissue. Furthermore, RMRP downregulation induced apoptotic cell death. RMRP is downregulated by PERK, which induces apoptosis in HCC. RMRP could be a new therapeutic target to regulate HCC in patients with chronic liver diseases associated with ER stress.Atsushi YukimotoTakao WatanabeKotaro SunagoYoshiko NakamuraTakaaki TanakaYohei KoizumiOsamu YoshidaYoshio TokumotoMasashi HirookaMasanori AbeYoichi HiasaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Atsushi Yukimoto Takao Watanabe Kotaro Sunago Yoshiko Nakamura Takaaki Tanaka Yohei Koizumi Osamu Yoshida Yoshio Tokumoto Masashi Hirooka Masanori Abe Yoichi Hiasa The long noncoding RNA of RMRP is downregulated by PERK, which induces apoptosis in hepatocellular carcinoma cells
description	Abstract Endoplasmic reticulum (ER) stress plays an important role in hepatocyte degeneration, especially in patients with chronic liver injury. Protein kinase R-like endoplasmic reticulum kinase (PERK) is a key molecule in ER stress. PERK may contribute to apoptotic cell death in HCC, however the details of the mechanism are not clear. In this study, we identified PERK-associated molecules using transcriptome analysis. We modulated PERK expression using a plasmid, tunicamycin and siRNA against PERK, and then confirmed the target gene expression with real-time PCR and Northern blotting. We further analyzed the apoptotic function. Transcriptome analysis revealed that expression of the RNA component of mitochondrial RNA processing endoribonuclease (RMRP), which is a long noncoding RNA, was strongly correlated with the function of PERK. The expression of RMRP was correlated with the expression of PERK in experiments with the siRNA and PERK plasmid in both HCC cell lines and human HCC tissue. Furthermore, RMRP downregulation induced apoptotic cell death. RMRP is downregulated by PERK, which induces apoptosis in HCC. RMRP could be a new therapeutic target to regulate HCC in patients with chronic liver diseases associated with ER stress.
format	article
author	Atsushi Yukimoto Takao Watanabe Kotaro Sunago Yoshiko Nakamura Takaaki Tanaka Yohei Koizumi Osamu Yoshida Yoshio Tokumoto Masashi Hirooka Masanori Abe Yoichi Hiasa
author_facet	Atsushi Yukimoto Takao Watanabe Kotaro Sunago Yoshiko Nakamura Takaaki Tanaka Yohei Koizumi Osamu Yoshida Yoshio Tokumoto Masashi Hirooka Masanori Abe Yoichi Hiasa
author_sort	Atsushi Yukimoto
title	The long noncoding RNA of RMRP is downregulated by PERK, which induces apoptosis in hepatocellular carcinoma cells
title_short	The long noncoding RNA of RMRP is downregulated by PERK, which induces apoptosis in hepatocellular carcinoma cells
title_full	The long noncoding RNA of RMRP is downregulated by PERK, which induces apoptosis in hepatocellular carcinoma cells
title_fullStr	The long noncoding RNA of RMRP is downregulated by PERK, which induces apoptosis in hepatocellular carcinoma cells
title_full_unstemmed	The long noncoding RNA of RMRP is downregulated by PERK, which induces apoptosis in hepatocellular carcinoma cells
title_sort	long noncoding rna of rmrp is downregulated by perk, which induces apoptosis in hepatocellular carcinoma cells
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/c81affd535aa44499e9b9374cdcaecf6
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The long noncoding RNA of RMRP is downregulated by PERK, which induces apoptosis in hepatocellular carcinoma cells

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