SIRT1 Expression Is Associated with Good Prognosis in Colorectal Cancer.
- Author:
Wonkyung JUNG
1
;
Kwang Dae HONG
;
Woon Yong JUNG
;
Eunjung LEE
;
Bong Kyung SHIN
;
Han Kyeom KIM
;
Aeree KIM
;
Baek Hui KIM
Author Information
1. Department of Pathology, Korea University Guro Hospital, Korea University College of Medicine, Seoul, Korea. maelstrom@naver.com
- Publication Type:Original Article
- Keywords:
Colon;
Adenocarcinoma;
SIRT1;
DBC1;
Beta catenin
- MeSH:
Adenocarcinoma;
beta Catenin;
Breast Neoplasms;
Colon;
Colorectal Neoplasms;
Humans;
Multivariate Analysis;
Oncogenes;
Prognosis;
Sirtuin 1
- From:Korean Journal of Pathology
2013;47(4):332-339
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Silent mating type information regulation 2 homolog 1 (SIRT1), an NAD+-dependent deacetylase, might act as a tumor promoter by inhibiting p53, but may also as a tumor suppressor by inhibiting several oncogenes such as beta-catenin and survivin. Deleted in breast cancer 1 (DBC1) is known as a negative regulator of SIRT1. METHODS: Immunohistochemical expressions of SIRT1, DBC1, beta-catenin, surviving, and p53 were evaluated using 2 mm tumor cores from 349 colorectal cancer patients for tissue microarray. RESULTS: Overexpression of SIRT1, DBC1, survivin, and p53 was seen in 235 (67%), 183 (52%), 193 (55%), and 190 (54%) patients, respectively. Altered expression of beta-catenin was identified in 246 (70%) patients. On univariate analysis, overexpression of SIRT1 (p=0.029) and altered expression of beta-catenin (p=0.008) were significantly associated with longer overall survival. Expression of SIRT1 was significantly related to DBC1 (p=0.001), beta-catenin (p=0.001), and survivin (p=0.002), but not with p53. On multivariate analysis, age, tumor stage, differentiation, and expression of SIRT1 were independent prognostic factors significantly associated with overall survival. CONCLUSIONS: SIRT1 overexpression is a good prognostic factor for colorectal cancer, and SIRT1 may interact with beta-catenin and survivin rather than p53.