## Abstract Lactotransferrin (LTF) has been shown to regulate tumorogenesis. However, little is known about the role of LTF in regulating the development of human nasopharyngeal carcinoma (NPC). The aim of our study was to investigate whether LTF could regulate the development of NPC by characteriz
NGX6 gene inhibits cell proliferation and plays a negative role in EGFR pathway in nasopharyngeal carcinoma cells
✍ Scribed by Lili Wang; Jian Ma; Jiang Li; Xiaoling Li; Qiuhong Zhang; Shuping Peng; Cong Peng; Ming Zhou; Wei Xiong; Jianbo Yang; Jie Zhou; Songqing Fan; Chen Tan; Qun Yan; Shourong Shen; Guiyuan Li
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 222 KB
- Volume
- 95
- Category
- Article
- ISSN
- 0730-2312
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Nasopharyngeal carcinoma (NPC) is a common cancer in South China but is rare in other parts of the world. A novel NPC‐related gene was isolated by location candidate cloning strategy, whose expression was down‐regulated in NPC. This gene was designated human NGX6 (Genbank accession AF188239) and encoded a predicted protein of 338 amino acids that harbors an EGF‐like domain. The effects of NGX6 on cells from human NPC cell line HNE1 were investigated. The cells transfected with NGX6 had a markedly high expression of NGX6, leading to significant decrease in cell proliferation and the capability to form colonies in soft agar, delaying the G~0~–G~1~ cell cycle progression. Flow cytometry assay indicated that the expression of cyclin D1 significantly decreased in NGX6‐transfected HNE1 cells as well as cyclin A and E. There was a delay in tumor formation and a dramatic reduction in tumor size when cells transfected with NGX6 were injected into nude mice. In another way, we found NGX6 played a negative role in EGFR Ras/Mek/MAPK pathway. We propose that NGX6, as an EGF‐like domain gene, could delay cell cycle G~0~–G~1~ progression and thus inhibit cell proliferation by negatively regulating EGFR pathway in NPC cells and down‐regulating the expression of cyclin D1 and E. © 2005 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES