Deregulation of lipid metabolism pathway genes in nasopharyngeal carcinoma cells

被引:51
作者
Daker, Maelinda [1 ]
Bhuvanendran, Saatheeyavaane [1 ]
Ahmad, Munirah [1 ]
Takada, Kenzo [2 ]
Khoo, Alan Soo-Beng [1 ]
机构
[1] Inst Med Res, Canc Res Ctr, Mol Pathol Unit, Kuala Lumpur 50588, Malaysia
[2] Hokkaido Univ, Inst Med Genet, Dept Tumour Virol, Sapporo, Hokkaido 0600815, Japan
关键词
Epstein-Barr virus-encoded RNAs; fatty acid synthase; lipid metabolism; low-density lipoprotein receptor; nasopharyngeal carcinoma; quercetin; DENSITY-LIPOPROTEIN RECEPTOR; FATTY-ACID SYNTHASE; PHARMACOLOGICAL INHIBITORS; FEEDBACK-REGULATION; HUMAN CANCER; T-CELLS; GROWTH; EXPRESSION; QUERCETIN; APOPTOSIS;
D O I
10.3892/mmr.2012.1253
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Nasopharyngeal carcinoma (NPC) is a unique tumour of epithelial origin with a distinct geographical distribution, closely associated with the Epstein-Barr virus (EBV). EBV-encoded RNAs (EBERs) are small non-polyadenylated RNAs that are abundantly expressed in latent EBV-infected NPC cells. To study the role of EBERs in NPC, we established stable expression of EBERs in HK1, an EBV-negative NPC cell line. Cells expressing EBERs consistently exhibited an increased growth rate. However, EBERs did not confer resistance towards cisplatin-induced apoptosis or promote migration or invasion ability in the cells tested. Using microarray gene expression profiling, we identified potential candidate genes that were deregulated in NPC cells expressing EBERs. Gene Ontology analysis of the data set revealed that EBERs upregulate the cellular lipid metabolic process. Upregulation of low-density lipoprotein receptor (LDLR) and fatty acid synthase (FASN) was observed in EBER-expressing cells. NPC cells exhibited LDL-dependent cell proliferation. In addition, a polyphenolic flavonoid compound, quercetin, known to inhibit FASN, was found to inhibit proliferation of NPC cells.
引用
收藏
页码:731 / 741
页数:11
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