FLJ10540 is associated with tumor progression in nasopharyngeal carcinomas and contributes to nasopharyngeal cell proliferation, and metastasis via osteopontin/CD44 pathway

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Title:	FLJ10540 is associated with tumor progression in nasopharyngeal carcinomas and contributes to nasopharyngeal cell proliferation, and metastasis via osteopontin/CD44 pathway
Authors:	蘇立仁;Chen, Chang-Han;Shiu, Li-Yen;Su, Li-Jen;Huang, Chi-Ying F;Huang, Shun-Chen;Huang, Chao-Cheng;Yin, Yu-Fang;Wang, Wei-Sheng;Tsai, Hsin-Ting;Fang, Fu-Min;Chuang, Wan-Chu;Kang, Hong-Chang;Hwang, Chung-Feng
Contributors:	生醫理工學院生醫科學與工程學系
Keywords:	Bioinformatics;Biomedical and Life Sciences;Biomedicine;Breast cancer;Cancer;Cancer microenvironment;Cancer therapies;Carcinoma;CD44;Cell Cycle Proteins - genetics;Cell Cycle Proteins - metabolism;Cell Line, Tumor;Cell Movement;Cell Proliferation;Chi-Square Distribution;Cytokines;Development and progression;Disease;Disease Progression;Down-Regulation - genetics;FLJ10540;Gene Expression Regulation, Neoplastic;Gene Knockdown Techniques;Genes, Neoplasm - genetics;Genetic aspects;Genetic research;Head & neck cancer;Hospitals;Humans;Immunohistochemistry;Medical imaging;Medicine;Medicine/Public Health;Metastasis;Nasopharyngeal cancer;Nasopharyngeal Carcinoma;Nasopharyngeal Neoplasms - genetics;Nasopharyngeal Neoplasms - pathology;Nasopharynx - metabolism;Nasopharynx - pathology;Neoplasm Invasiveness;Neoplasm Metastasis;Nuclear Proteins - genetics;Nuclear Proteins - metabolism;Osteopontin;Osteopontin - genetics;Osteopontin - metabolism;Otolaryngology;Pathology;Phosphoproteins;Physiological aspects;Prognosis;Proportional Hazards Models;Proteins;Radiation therapy;RNA;RNA, Small Interfering - metabolism;Rodents;Signal Transduction - genetics;Survival Analysis;Transfection;University colleges;Up-Regulation - genetics
Date:	2012-05-16
Issue Date:	2026-04-23 11:16:06 (UTC+8)
Publisher:	BioMed Central Ltd.;London: BioMed Central
Abstract:	摘要： Background Nasopharyngeal carcinoma (NPC) is well-known for its highly metastatic characteristics, but little is known of its molecular mechanisms. New biomarkers that predict clinical outcome, in particular the ability of the primary tumor to develop metastatic tumors are urgently needed. The aim of this study is to investigate the role of FLJ10540 in human NPC development. Methods A bioinformatics approach was used to explore the potentially important regulatory genes involved in the growth/metastasis control of NPC. FLJ10540 was chosen for this study. Two co-expression strategies from NPC microarray were employed to identify the relationship between FLJ10540 and osteopontin. Quantitative-RT-PCR, immunoblotting, and immunohistochemistry analysis were used to investigate the mRNA and protein expression profiles of FLJ10540 and osteopontin in the normal and NPC tissues to confirm microarray results. TW01 and Hone1 NPC cells with overexpression FLJ10540 or siRNA to repress endogenous FLJ10540 were generated by stable transfection to further elucidate the molecular mechanisms of FLJ10540-elicited cell growth and metastasis under osteopontin stimulation. Results We found that osteopontin expression exhibited a positive correlation with FLJ10540 in NPC microarray. We also demonstrated comprehensively that FLJ10540 and osteopontin were not only overexpressed in NPC specimens, but also significantly correlated with advanced tumor and lymph node-metastasis stages, and had a poor 5-year survival rate, respectively. Stimulation of NPC parental cells with osteopontin results in an increase in FLJ10540 mRNA and protein expressions. Functionally, FLJ10540 transfectant alone, or stimulated with osteopontin, exhibited fast growth and increased metastasis as compared to vehicle control with or without osteopontin stimulation. Conversely, knockdown of FLJ10540 by siRNA results in the suppression of NPC cell growth and motility. Treatment with anti-CD44 antibodies in NPC parental cells not only resulted in a decrease of FLJ10540 protein, but also affected the abilities of FLJ10540-elicited cell growth and motility in osteopontin stimulated-NPC cells. Conclusions These findings suggest that FLJ10540 may be critical regulator of disease progression in NPC, and the underlying mechanism may involve in the osteopontin/CD44 pathway. 其他題名： J Transl Med 出版者： London: BioMed Central 出版日期： 2012-05-16 出處： Journal of translational medicine, 2012-05, Vol.10 (1), p.93-93, Article 93 資源來源： ProQuest Open Access Content Collection 版權： Chen et al.; licensee BioMed Central Ltd. 2012 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 版權： COPYRIGHT 2012 BioMed Central Ltd. 版權： 2012 Chen et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 版權： Copyright ©2012 Chen et al.; licensee BioMed Central Ltd. 2012 Chen et al.; licensee BioMed Central Ltd. 識別號： ISSN: 1479-5876 識別號： EISSN: 1479-5876 識別號： DOI: 10.1186/1479-5876-10-93 識別號： PMID: 22591637
Appears in Collections:	[Department of Biomedical Sciences and Engineering ] journal & Dissertation

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