Downregulation of runt‐related transcription factor 3 associated with poor prognosis of adenoid cystic and mucoepidermoid carcinomas of the salivary gland
Downregulation of runt‐related transcription factor 3 associated with poor prognosis of adenoid cystic and mucoepidermoid carcinomas of the salivary gland
复制标题
runt相关转录因子3的下调与唾液腺腺样囊性癌和粘液表皮样癌的不良预后相关
DOI:
10.1111/j.1349-7006.2010.01787.x
复制
发表时间:
2011
期刊:
影响因子:
5.7
通讯作者:
H. Kuniyasu
中科院分区:
文献类型:
--
作者:
T. Sasahira;Miyako Kurihara;Kazuhiko Yamamoto;U. Bhawal;T. Kirita;H. Kuniyasu
Runt‐related transcription factor 3 (RUNX3) is a transcription factor of the transforming growth factor (TGF)‐β superfamily and acts as a tumor suppressor gene, which is silenced by hypermethylation of the promoter region in various cancers. In this study, we examined the expression and methylation status of RUNX3 in the salivary gland cancers pleomorphic adenoma (PA), adenoid cystic carcinoma (ACC) and mucoepidermoid carcinoma (MEC). The cytoplasmic expression rates of RUNX3 in PA, ACC and MEC were 65% (13/20), 22.2% (8/36) and 20.6% (7/34), respectively. Low expression or deletion of RUNX3 in ACC and MEC was significantly associated with tumor progression and poor prognosis. Using microdissected cDNA, we found that RUNX3 mRNA expression was lower in ACC and MEC than in PA and noncancerous salivary glands; furthermore, hypermethylation of RUNX3 was detected more frequently in PA (2/8, 25%), ACC (6/8, 75%) and MEC (7/8, 87.5%) than in noncancerous salivary glands (0/8, 0%). Our results suggest that low expression or deletion of RUNX3 in salivary gland tumors might play a pivotal role in tumorigenesis and tumor progression and poor prognosis in the case of salivary gland ACC and MEC. Recovery of the tumor suppressive function of RUNX3 might inhibit tumorigenesis and cancer progression in the human salivary gland. (Cancer Sci 2011; 102: 492–497)
影响因子:
11.2
作者:
G. Barnes;A. Javed;Sylvan M Waller;M. Kamal;Kerri E Hebert;Mohammad Q. Hassan;A. Bellahcène;A. V.
通讯作者:
G. Barnes;A. Javed;Sylvan M Waller;M. Kamal;Kerri E Hebert;Mohammad Q. Hassan;A. Bellahcène;A. V.