Smad4 mediates malignant behaviors of human ovarian carcinoma cell through the effect on expressions of E-cadherin, plasminogen activator inhibitor-1 and VEGF

被引:25
作者
Chen, Chen [1 ,2 ]
Sun, Ming-Zhon [1 ]
Liu, Shuqing [1 ]
Yeh, Dongmei [1 ,2 ]
Yu, Lijun [1 ]
Song, Yang [1 ]
Gong, Linlin [1 ]
Hao, Lihong [1 ]
Hu, Jun [1 ]
Shao, Shujuan [1 ]
机构
[1] Dalian Med Univ, Key Lab Prote Liaoning Prov, Dalian 116044, Peoples R China
[2] Dalian Univ, Dept Anat, Dalian 116044, Peoples R China
基金
中国国家自然科学基金;
关键词
Invasion; Ovarian cancer; Progression; Smad4; Tumor metastasis; UROKINASE RECEPTOR; CANCER; METASTASIS; APOPTOSIS; PATTERNS; ADHESION; INVASION; GENE;
D O I
10.5483/BMBRep.2010.43.8.554
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Smad4 is involved in cancer progression and metastasis. Using a pair of human syngeneic epithelial ovarian cancer cells with low (HO-8910) and high (HO-8910PM) metastatic abilities, we aimed to reveal the role of Smad4 in ovarian cancer metastasis in vitro. Smad4 was down-regulated in HO-8910PM cell line relative to HO-8910 by implicating Smad4 was probably a potential tumor suppressor gene for ovarian cancer. Re-expression of Smad4 decreased the migration ability and inhibited the invasion capacity of HO-8910PM, while promoted the cell adhesion capacity for HO-8910PM. The stable expression of Smad4 increased the expression of E-cadherin, reduced the expression of plasminogen activator inhibitor-1 (PAI-1) and slightly down-regulated the expression of VEGF. Smad4 suppresses human ovarian cancer cell metastasis potential through its effect on the expressions of PAI-1, E-cadherin and VEGF. Results from current work implicate Smad4 might suppress the invasion and metastasis of human ovarian tumor cells through a TGF-beta/Smad-mediated pathway. [BMB reports 2010; 43(8): 554-560]
引用
收藏
页码:554 / 560
页数:7
相关论文
共 30 条
[1]
CANCER: Blood vessels kept quiet [J].
Benest, Andrew V. ;
Augustin, Hellmut G. .
NATURE, 2009, 458 (7234) :41-42
[2]
TGF-β-induced fibroblast activation protein expression, fibroblast activation protein expression increases the proliferation, adhesion, and migration of HO-8910PM [J].
Chen, He ;
Yang, Wei-Wei ;
Wen, Qiu-Ting ;
Xu, Li ;
Chen, Ming .
EXPERIMENTAL AND MOLECULAR PATHOLOGY, 2009, 87 (03) :189-194
[3]
VEGF inhibition: insights from preclinical and clinical studies [J].
Crawford, Yongping ;
Ferrara, Napoleone .
CELL AND TISSUE RESEARCH, 2009, 335 (01) :261-269
[4]
TWEAK promotes ovarian cancer cell metastasis via NF-κB pathway activation and VEGF expression [J].
Dai, Lan ;
Gu, Liying ;
Ding, Chuanwei ;
Qiu, Lihua ;
Di, Wen .
CANCER LETTERS, 2009, 283 (02) :159-167
[5]
Gutierrez LS, 2000, CANCER RES, V60, P5839
[6]
DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1 [J].
Hahn, SA ;
Schutte, M ;
Hoque, ATMS ;
Moskaluk, CA ;
daCosta, LT ;
Rozenblum, E ;
Weinstein, CL ;
Fischer, A ;
Yeo, CJ ;
Hruban, RH ;
Kern, SE .
SCIENCE, 1996, 271 (5247) :350-353
[7]
HEALY AM, 1994, J BIOL CHEM, V269, P19095
[8]
Two distinct expression patterns of urokinase, urokinase receptor and plasminogen activator inhibitor-1 in colon cancer liver metastases [J].
Illemann, Martin ;
Bird, Nigel ;
Majeed, Ali ;
Laerum, Ole D. ;
Lund, Leif R. ;
Dano, Keld ;
Nielsen, Boye Schnack .
INTERNATIONAL JOURNAL OF CANCER, 2009, 124 (08) :1860-1870
[9]
Nucleocytoplasmic shuttling of Smads 2, 3, and 4 permits sensing of TGF-β receptor activity [J].
Inman, GJ ;
Nicolás, FJ ;
Hill, CS .
MOLECULAR CELL, 2002, 10 (02) :283-294
[10]
A New Target for Tumor Therapy [J].
Jain, Rakesh K. .
NEW ENGLAND JOURNAL OF MEDICINE, 2009, 360 (25) :2669-2671