Role of reduced expression of SMAD4 in papillary thyroid carcinoma

被引：21

作者：

D'Inzeo, Sonia ^{[1
]}

Nicolussi, Arianna ^{[1
]}

Ricci, Antonella ^{[1
]}

Mancini, Patrizia ^{[1
]}

Porcellini, Antonio ^{[2
]}

Nardi, Francesco ^{[1
]}

Coppa, Anna ^{[1
]}

机构：

[1] Univ Roma La Sapienza, Dept Expt Med, I-00161 Rome, Italy

[2] Univ Molise, Dept Hlth Sci, I-86100 Campobasso, Italy

来源：

JOURNAL OF MOLECULAR ENDOCRINOLOGY | 2010年 / 45卷 / 04期

关键词：

GROWTH-FACTOR-BETA; TUMOR-NECROSIS-FACTOR; TGF-BETA; TRANSFORMING GROWTH-FACTOR-BETA-1; E-CADHERIN; CELL-LINE; TRANSCRIPTIONAL ACTIVATION; EPITHELIAL-CELLS; GENE-EXPRESSION; ACTIVIN-A;

D O I：

10.1677/JME-10-0044

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

It has been demonstrated that transforming growth factor-beta (TGF beta) and other members of TGF beta superfamily play an important role in thyroid proliferative diseases. The deficiencies of SMAD4 are responsible to accelerate the malignant progression of neoplastic lesions in several types of tumors. Therefore, the objective of the present study was to determine the functional role of reduced expression of SMAD4 in human papillary thyroid carcinogenesis. For this purpose, we examined the TGF beta response in two cell lines, TPC-1 and BCPAP. Our data demonstrated for the first time that these cells showed a strong reduction in the level of SMAD4 protein, which was responsible for an alteration of TGF beta signaling and for some of the TGF beta-mediated biological effects. The overexpression of SMAD4, restoring TGF beta transduction, determined a significant increase of antiproliferative response to TGF beta, and reduced the invasive behavior of these cells. Therefore, our data indicated that reduction of SMAD4 may play a significant role in thyroid carcinogenesis. Journal of Molecular Endocrinology (2010) 45, 229-244

引用

页码：229 / 244

页数：16

共 76 条

[1]

CULTURE OF HORMONE-DEPENDENT FUNCTIONAL EPITHELIAL-CELLS FROM RAT THYROIDS [J].

AMBESIIMPIOMBATO, FS ;

PARKS, LAM ;

COON, HG .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1980, 77 (06) :3455-3459

[2]

Smads as transcriptional co-modulators [J].

Attisano, L ;

Wrana, JL .

CURRENT OPINION IN CELL BIOLOGY, 2000, 12 (02) :235-243

[3]

Expression of matrix metalloproteinases and their specific inhibitors in normal and different human thyroid tumor cell lines [J].

Baldini, E ;

Toller, M ;

Graziano, FM ;

Russo, FP ;

Pepe, M ;

Biordi, L ;

Marchioni, E ;

Curcio, F ;

Ulisse, S ;

Ambesi-Impiombato, FS ;

D'Armiento, M .

THYROID, 2004, 14 (11) :881-888

[4]

Growth factors and goitrogenesis [J].

Bidey, SP ;

Hill, DJ ;

Eggo, MC .

JOURNAL OF ENDOCRINOLOGY, 1999, 160 (03) :321-332

[5]

TYPE-I RECEPTORS SPECIFY GROWTH-INHIBITORY AND TRANSCRIPTIONAL RESPONSES TO TRANSFORMING GROWTH-FACTOR-BETA AND ACTIVIN [J].

CARCAMO, J ;

WEIS, FMB ;

VENTURA, F ;

WIESER, R ;

WRANA, JL ;

ATTISANO, L ;

MASSAGUE, J .

MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (06) :3810-3821

[6]

TGF-β1 actions on FRTL-5 cells provide a model for the physiological regulation of thyroid growth [J].

Carneiro, C ;

Alvarez, CV ;

Zalvide, J ;

Vidal, A ;

Domínguez, F .

ONCOGENE, 1998, 16 (11) :1455-1465

[7]

Expression of Smad4 and Smad7 in human thyroid follicular carcinoma cell lines [J].

Cerutti, JM ;

Ebina, KN ;

Matsuo, SE ;

Martins, L ;

Maciel, RMB ;

Kimura, ET .

JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION, 2003, 26 (06) :516-521

[8]

Molecular Origins of Cancer Molecular Basis of Metastasis [J].

Chiang, Anne C. ;

Massague, Joan .

NEW ENGLAND JOURNAL OF MEDICINE, 2008, 359 (26) :2814-2823

[9]

New signals from the invasive front [J].

Christofori, G .

NATURE, 2006, 441 (7092) :444-450

[10]

COLLETTA G, 1989, CANCER RES, V49, P3457

← 1 2 3 4 5 6 7 8 →