DEAD-box Helicase 27 Promotes Hepatocellular Carcinoma Progression Through ERK Signaling

Introduction: DEAD-box helicase 27 (DDX27) belongs to DEAD-Box nucleic acid helicase family. The function of DDX27 in hepatocellular carcinoma (HCC) remain enigmatic. In light of this, we tried to investigate the regulatory role and underlying mechanism of DDX27 in HCC. Materials and methods: DDX27...

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Autores principales:	Wang Xiaoqian, Zhang Bing, Li Yangwei, Zhi Yafei, Zhang Tingting, Wang Yi, Li Qingjun, Luo Suxia, Zhang Ling, Wang Bo, Zheng Peng
Formato:	article
Lenguaje:	EN
Publicado:	SAGE Publishing 2021
Materias:	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/945802566c8346858736cb3217734d8f
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spelling	oai:doaj.org-article:945802566c8346858736cb3217734d8f2021-12-03T00:03:28ZDEAD-box Helicase 27 Promotes Hepatocellular Carcinoma Progression Through ERK Signaling1533-033810.1177/15330338211055953https://doaj.org/article/945802566c8346858736cb3217734d8f2021-12-01T00:00:00Zhttps://doi.org/10.1177/15330338211055953https://doaj.org/toc/1533-0338Introduction: DEAD-box helicase 27 (DDX27) belongs to DEAD-Box nucleic acid helicase family. The function of DDX27 in hepatocellular carcinoma (HCC) remain enigmatic. In light of this, we tried to investigate the regulatory role and underlying mechanism of DDX27 in HCC. Materials and methods: DDX27 expression levels were detected by qRT-PCR, Western blot and immunohistochemistry assays in HCC tissues and cells. Colony formation, CCK-8, growth curve, wound healing and transwell assays were conducted to investigate the effect of DDX27 on the proliferation and metastasis of HCC cells. RNA-sequencing was performed to detect the effect of DDX27 on downstream signaling pathway. The effect of DDX27 on HCC progression was evaluated using in vivo murine xenograft model. Results: we found an increased expression of DDX27 in HCC tissues with comparison to its para-tumor tissues. The high expression levels of DDX27 were associated with poor prognosis in HCC patients. DDX27 upregulation promoted cell metastasis. Mechanistic studies suggested that DDX27 overexpression induces the major vault protein (MVP) expression and enhances the phosphorylation levels of ERK1/2. Inhibition of ERK pathway impaired the cellular metastastic abilities induced by DDX27. The induction of DDX27 in HCC progression was further confirmed from tumors in mouse model. Conclusion: our results disclose a novel mechanism by which DDX27 enhances ERK signaling during HCC progression. DDX27 might be used in targeted therapy for HCC patients.Wang XiaoqianZhang BingLi YangweiZhi YafeiZhang TingtingWang YiLi QingjunLuo SuxiaZhang LingWang BoZheng PengSAGE PublishingarticleNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENTechnology in Cancer Research & Treatment, Vol 20 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Wang Xiaoqian Zhang Bing Li Yangwei Zhi Yafei Zhang Tingting Wang Yi Li Qingjun Luo Suxia Zhang Ling Wang Bo Zheng Peng DEAD-box Helicase 27 Promotes Hepatocellular Carcinoma Progression Through ERK Signaling
description	Introduction: DEAD-box helicase 27 (DDX27) belongs to DEAD-Box nucleic acid helicase family. The function of DDX27 in hepatocellular carcinoma (HCC) remain enigmatic. In light of this, we tried to investigate the regulatory role and underlying mechanism of DDX27 in HCC. Materials and methods: DDX27 expression levels were detected by qRT-PCR, Western blot and immunohistochemistry assays in HCC tissues and cells. Colony formation, CCK-8, growth curve, wound healing and transwell assays were conducted to investigate the effect of DDX27 on the proliferation and metastasis of HCC cells. RNA-sequencing was performed to detect the effect of DDX27 on downstream signaling pathway. The effect of DDX27 on HCC progression was evaluated using in vivo murine xenograft model. Results: we found an increased expression of DDX27 in HCC tissues with comparison to its para-tumor tissues. The high expression levels of DDX27 were associated with poor prognosis in HCC patients. DDX27 upregulation promoted cell metastasis. Mechanistic studies suggested that DDX27 overexpression induces the major vault protein (MVP) expression and enhances the phosphorylation levels of ERK1/2. Inhibition of ERK pathway impaired the cellular metastastic abilities induced by DDX27. The induction of DDX27 in HCC progression was further confirmed from tumors in mouse model. Conclusion: our results disclose a novel mechanism by which DDX27 enhances ERK signaling during HCC progression. DDX27 might be used in targeted therapy for HCC patients.
format	article
author	Wang Xiaoqian Zhang Bing Li Yangwei Zhi Yafei Zhang Tingting Wang Yi Li Qingjun Luo Suxia Zhang Ling Wang Bo Zheng Peng
author_facet	Wang Xiaoqian Zhang Bing Li Yangwei Zhi Yafei Zhang Tingting Wang Yi Li Qingjun Luo Suxia Zhang Ling Wang Bo Zheng Peng
author_sort	Wang Xiaoqian
title	DEAD-box Helicase 27 Promotes Hepatocellular Carcinoma Progression Through ERK Signaling
title_short	DEAD-box Helicase 27 Promotes Hepatocellular Carcinoma Progression Through ERK Signaling
title_full	DEAD-box Helicase 27 Promotes Hepatocellular Carcinoma Progression Through ERK Signaling
title_fullStr	DEAD-box Helicase 27 Promotes Hepatocellular Carcinoma Progression Through ERK Signaling
title_full_unstemmed	DEAD-box Helicase 27 Promotes Hepatocellular Carcinoma Progression Through ERK Signaling
title_sort	dead-box helicase 27 promotes hepatocellular carcinoma progression through erk signaling
publisher	SAGE Publishing
publishDate	2021
url	https://doaj.org/article/945802566c8346858736cb3217734d8f
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DEAD-box Helicase 27 Promotes Hepatocellular Carcinoma Progression Through ERK Signaling

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