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Title: Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation
Author: Wang, Hanzhi ; Xiao, Wei ; Zhou, Qinbo ; Chen, Yun ; Yang, Shuo ; Sheng, Jiansong ; Yin, Yanqing ; Fan, Jia ; null(周嘉伟)
Source: CELL RESEARCH
Issued Date: 2009
Volume: 19, Issue:10, Pages:1150-1164
Keyword: 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
Subject: Cell Biology
Corresponding Author: 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
English Abstract: 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.
Indexed Type: sci
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/1636
Appears in Collections:神经所(总)_期刊论文
基底神经节的发育与退行性疾病研究组_期刊论文

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Wang, Hanzhi; Xiao, Wei; Zhou, Qinbo; Chen, Yun; Yang, Shuo; Sheng, Jiansong; Yin, Yanqing; Fan, Jia; Zhou, Jiawei.Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation,CELL RESEARCH,2009,19(10):1150-1164
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