Influence of thyroid hormone receptors on breast cancer cell proliferation

被引:76
作者
Conde, I
Paniagua, R
Zamora, J
Blánquez, MJ
Fraile, B
Ruiz, A
Arenas, MI [1 ]
机构
[1] Univ Alcala De Henares, Dept Cell Biol & Genet, Madrid 28871, Spain
[2] Hosp Ramon & Cajal, Clin Biostat Unit, E-28034 Madrid, Spain
[3] Univ Complutense, Sch Vet, Dept Anat, E-28040 Madrid, Spain
[4] Hosp Principe Asturias, Dept Pathol, Madrid 28805, Spain
关键词
breast; cancer; proliferation; thyroid hormone receptors;
D O I
10.1093/annonc/mdj040
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Background: The involvement of thyroid hormones in the development and differentiation of normal breast tissue has been established. However, the association between breast cancer and these hormones is controversial. Therefore, the objective of the present study was to determine the protein expression pattern of thyroid hormone receptors in different human breast pathologies and to evaluate their possible relationship with cellular proliferation. Patients and methods: The presence of thyroid hormone receptors was evaluated by immunohistochemistry and western blot analysis in 84 breast samples that included 12 cases of benign proliferative diseases, 20 carcinomas in situ and 52 infiltrative carcinomas. Results: TR-alpha was detected in the nuclei of epithelial cells from normal breast ducts and acini, while in any pathological type this receptor was located in the cytoplasm. However, TR-beta presented a nuclear location in benign proliferative diseases and carcinomas in situ and a cytoplasmatic location in normal breast and infiltrative carcinomas. The highest proliferation index was observed in carcinomas in situ, although in infiltrative carcinomas an inverse correlation between this index and the TR-alpha expression was encountered. Conclusions: The results of this study reveal substantial changes in the expression profile of thyroid hormone receptors suggesting a possible deregulation that could trigger breast cancer development.
引用
收藏
页码:60 / 64
页数:5
相关论文
共 26 条
[1]
ALVARADOPISANI AR, 1986, ANTICANCER RES, V6, P1347
[2]
Beatson GT., 1896, LANCET, V148, P104, DOI DOI 10.1016/S0140-6736(01)72307-0
[3]
BURKE RE, 1978, CANCER RES, V38, P3769
[4]
Construction of a cyclin D1-Cdk2 fusion protein to model the biological functions of cyclin D1-Cdk2 complexes [J].
Chytil, A ;
Waltner-Law, M ;
West, R ;
Friedman, D ;
Aakre, M ;
Barker, D ;
Law, B .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (46) :47688-47698
[5]
EVALUATION OF PROLIFERATING CELL NUCLEAR ANTIGEN (PCNA) AS AN ENDOGENOUS MARKER OF CELL-PROLIFERATION IN RAT-LIVER - A DUAL-STAIN COMPARISON WITH 5-BROMO-2'-DEOXYURIDINE [J].
CONNOLLY, KM ;
BOGDANFFY, MS .
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 1993, 41 (01) :1-6
[6]
Thyroid disease: pathophysiology and diagnosis [J].
Demers, LM .
CLINICS IN LABORATORY MEDICINE, 2004, 24 (01) :19-+
[7]
Fasco M J, 2000, Mol Cell Endocrinol, V166, P156
[8]
FEI ZL, 1992, ENDOCRINOLOGY, V130, P1145
[9]
The thyroid hormone receptor is a suppressor of ras-mediated transcription, proliferation, and transformation [J].
García-Silva, S ;
Aranda, A .
MOLECULAR AND CELLULAR BIOLOGY, 2004, 24 (17) :7514-7523
[10]
Thyroid hormone receptors/THR genes in human cancer [J].
González-Sancho, JM ;
García, V ;
Bonilla, M ;
Muñoz, A .
CANCER LETTERS, 2003, 192 (02) :121-132