Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation

	Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation
	Wang, HZ; Xiao, W; Zhou, QB; Chen, Y; Yang, S; Sheng, JS; Yin, YQ; Fan, J; Zhou, JW
刊名	CELL RESEARCH
	2009
卷号	19 期号:10 页码:1150-1164
关键词	Bystin-like nucleologenesis nucleolar proteins cell growth hepatocellular carcinoma
通讯作者	Zhou, JW (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Mol Cell Biol Lab, Shanghai 200031, Peoples R China.,jwzhou@ion.ac.cn
英文摘要	The bystin-like (BYSL) gene was previously characterized to encode an accessory protein for cell adhesion that participates in early embryo implantation. It is also involved in 40S ribosomal subunit biogenesis and is found to be expressed in rapidly growing embryo and cancer cell lines. In order to explore the role of BYSL in cancer cell proliferation and growth, we used hepatocellular carcinoma (HCC) as a model. Here, we report that BYSL is crucial for HCC cell growth both in vitro and in vivo. Expression levels of BYSL mRNA and protein in human HCC specimens were markedly increased compared with those seen in adjacent non-cancerous tissue. In vitro, inhibition of BYSL by short hairpin RNA decreased HCC cell proliferation, induced apoptosis and partially arrested the cell cycle in the G2/M phase. In vivo, HCC cells treated with BYSL siRNA failed to form tumors in nude mice after subcutaneous implantation. To determine the cellular basis for BYSL RNAi-induced cell growth arrest, BYSL subcellular localization in mitotic and interphase HepG2 cells was examined. BYSL was present at multiple stages during nucleologenesis, including in nucleolus-derived foci (NDF), perichromosomal regions and the prenucleolar body (PNB) during mitosis. BYSL depletion remarkably suppressed NDF and PNB formation, and disrupted nucleoli assembly after mitosis, resulting in increased apoptosis and reduced tolerance of HCC cells to serum starvation. Taken together, our studies indicate that upregulated BYSL expression plays a role in hepatocarcinogenesis.
学科主题	Cell Biology
类目[WOS]	Cell Biology
关键词[WOS]	PRE-RIBOSOMAL-RNA ; ENDOMETRIAL EPITHELIAL-CELLS ; C-MYC AMPLIFICATION ; PRENUCLEOLAR BODIES ; LIVING CELLS ; U3 SNRNA ; EXPRESSION ; NUCLEOLUS ; TROPHININ ; MITOSIS
收录类别	SCI
语种	英语
WOS记录号	WOS:000270527600004
内容类型	期刊论文
版本	出版稿
源URL	[http://202.127.25.143/handle/331003/1247]
专题	上海生化细胞研究所_上海生科院生化细胞研究所
推荐引用方式 GB/T 7714	Wang, HZ,Xiao, W,Zhou, QB,et al. Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation[J]. CELL RESEARCH,2009,19(10):1150-1164.
APA	Wang, HZ.,Xiao, W.,Zhou, QB.,Chen, Y.,Yang, S.,...&Zhou, JW.(2009).Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation.CELL RESEARCH,19(10),1150-1164.
MLA	Wang, HZ,et al."Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation".CELL RESEARCH 19.10(2009):1150-1164.