NP9 gene inhibits tumorigenicity of nasopharyngeal carcinoma.
- Author:
Qi-cai LIU
1
;
Xiao-yan LI
;
Ba-xiong WEI
;
Yi-xin ZENG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cyclin D1; biosynthesis; genetics; Endogenous Retroviruses; genetics; Female; Gene Products, env; biosynthesis; genetics; Genes, Tumor Suppressor; Humans; Male; Mice; Mice, Inbred BALB C; Mice, Nude; Nasopharyngeal Neoplasms; genetics; metabolism; pathology; Neoplasm Transplantation; Proliferating Cell Nuclear Antigen; biosynthesis; genetics; Tumor Cells, Cultured
- From: Chinese Journal of Oncology 2005;27(11):641-644
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of NP9 on the growth of transplanted nasopharyngeal carcinoma (NPC) in nude mice and explore the mechanisms involved.
METHODSRecombinant pRc/CMV2-NP9 plasmid was constructed and transfected into the NPC cell lines by lipofectamine 2000. Cell clones stably expressing NP9 were obtained by detecting the mRNA expression of NP9 in G418-resistant clones with RT-PCR. The tumorigenicity and size of transplanted tumors were assessed after inoculation of NPC cells and their transgene clones into Balb/C mice. The expression of PCNA and cyclin D1 in transplanted tumors was detected by immunohistochemistry.
RESULTSThe expression of NP9 was detected in some of NP9 gene-transfected G418-resistant clones of CNE1 and SUNE1. In vivo experiments showed that the tumorigenicity of CNE19 clone was decreased significantly compared to that of CNE1 and its vector control, and the transplanted tumors grew more slowly from SUNE1/NP9 than from SUNE1 and SUNE1/vector. Compared with the vector control, the expression of cyclin D1 and PCNA in CNE1/NP9 transplants was decreased.
CONCLUSIONNP9 inhibits tumorigenicity and growth of NPC transplanted tumor by down-regulating the expression of cyclin D1 and PCNA.
