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

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	Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation
	Zhou, Jiawei
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 PRE-RIBOSOMAL-RNA ENDOMETRIAL EPITHELIAL-CELLS C-MYC AMPLIFICATION PRENUCLEOLAR BODIES LIVING CELLS U3 SNRNA EXPRESSION NUCLEOLUS TROPHININ MITOSIS
ISSN号	1001-0602
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
收录类别	SCI
资助信息	Chinese Academy of Sciences; National Natural Science Foundation of China[30525041, 30623003]; State Key Program for Basic Research of China[2006CB500704]
语种	英语
公开日期	2012-07-13
内容类型	期刊论文
源URL	[http://ir.sibs.ac.cn/handle/331001/1636]
专题	上海神经科学研究所_神经所(总) 上海神经科学研究所_基底神经节的发育与退行性疾病研究组
推荐引用方式 GB/T 7714	Zhou, Jiawei. 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	Zhou, Jiawei.(2009).Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation.CELL RESEARCH,19(10),1150-1164.
MLA	Zhou, Jiawei."Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation".CELL RESEARCH 19.10(2009):1150-1164.