The PDZ protein TIP-1 facilitates cell migration and pulmonary metastasis of human invasive breast cancer cells in athymic mice

Miaojun Han; Hailun Wang; Hua Tang Zhang; Zhaozhong Han

doi:10.1016/j.bbrc.2012.04.123

The PDZ protein TIP-1 facilitates cell migration and pulmonary metastasis of human invasive breast cancer cells in athymic mice

Miaojun Han, Hailun Wang, Hua Tang Zhang, Zhaozhong Han

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

Abstract

Tax-interacting protein 1 (TIP-1, also known as Tax1bp3) inhibited proliferation of colon cancer cells through antagonizing the transcriptional activity of beta-catenin. However, in this study, elevated TIP-1 expression levels were detected in human invasive breast cancers. Studies with two human invasive breast cancer cell lines indicated that RNAi-mediated TIP-1 knockdown suppressed the cell adhesion, proliferation, migration and invasion in vitro, and inhibited tumor growth in mammary fat pads and pulmonary metastasis in athymic mice. Biochemical studies showed that TIP-1 knockdown had moderate and differential effects on the beta-catenin-regulated gene expression, but remarkably down regulated the genes for cell adhesion and motility in breast cancer cells. The decreased expression of integrins and paxillin was accompanied with reduced cell adhesion and focal adhesion formation on fibronectin-coated surface. In conclusion, this study revealed a novel oncogenic function of TIP-1 suggesting that TIP-1 holds potential as a prognostic biomarker and a therapeutic target in the treatment of human invasive breast cancers.

Original language	English (US)
Pages (from-to)	139-145
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	422
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2012.04.123
State	Published - May 25 2012
Externally published	Yes

Keywords

Beta-catenin
Breast cancer
Cell adhesion
Migration
Pulmonary metastasis
Tax-interacting protein 1

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2012.04.123

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title = "The PDZ protein TIP-1 facilitates cell migration and pulmonary metastasis of human invasive breast cancer cells in athymic mice",

abstract = "Tax-interacting protein 1 (TIP-1, also known as Tax1bp3) inhibited proliferation of colon cancer cells through antagonizing the transcriptional activity of beta-catenin. However, in this study, elevated TIP-1 expression levels were detected in human invasive breast cancers. Studies with two human invasive breast cancer cell lines indicated that RNAi-mediated TIP-1 knockdown suppressed the cell adhesion, proliferation, migration and invasion in vitro, and inhibited tumor growth in mammary fat pads and pulmonary metastasis in athymic mice. Biochemical studies showed that TIP-1 knockdown had moderate and differential effects on the beta-catenin-regulated gene expression, but remarkably down regulated the genes for cell adhesion and motility in breast cancer cells. The decreased expression of integrins and paxillin was accompanied with reduced cell adhesion and focal adhesion formation on fibronectin-coated surface. In conclusion, this study revealed a novel oncogenic function of TIP-1 suggesting that TIP-1 holds potential as a prognostic biomarker and a therapeutic target in the treatment of human invasive breast cancers.",

keywords = "Beta-catenin, Breast cancer, Cell adhesion, Migration, Pulmonary metastasis, Tax-interacting protein 1",

author = "Miaojun Han and Hailun Wang and Zhang, {Hua Tang} and Zhaozhong Han",

note = "Funding Information: This study was supported in part by NIH Grants R01CA127482 (Z. Han), P50CA128323 (J. Gore) and the Vanderbilt CTSA Grant RR024975-01 from NCRR/NIH. We thank Dr. Jennifer Pietenpol at Vanderbilt-Ingram Cancer Center for the kind gift of human breast cancer cell line BT549. We appreciate the technical assistance and advices from Dr. Ling Geng (Pathology, Vanderbilt University) in the animal studies, and the excellent technical services at the Cell Imaging, Histology, and Genomics Cores at the Vanderbilt-Ingram Cancer Center. ",

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T1 - The PDZ protein TIP-1 facilitates cell migration and pulmonary metastasis of human invasive breast cancer cells in athymic mice

AU - Han, Miaojun

AU - Wang, Hailun

AU - Zhang, Hua Tang

AU - Han, Zhaozhong

N1 - Funding Information: This study was supported in part by NIH Grants R01CA127482 (Z. Han), P50CA128323 (J. Gore) and the Vanderbilt CTSA Grant RR024975-01 from NCRR/NIH. We thank Dr. Jennifer Pietenpol at Vanderbilt-Ingram Cancer Center for the kind gift of human breast cancer cell line BT549. We appreciate the technical assistance and advices from Dr. Ling Geng (Pathology, Vanderbilt University) in the animal studies, and the excellent technical services at the Cell Imaging, Histology, and Genomics Cores at the Vanderbilt-Ingram Cancer Center.

PY - 2012/5/25

Y1 - 2012/5/25

N2 - Tax-interacting protein 1 (TIP-1, also known as Tax1bp3) inhibited proliferation of colon cancer cells through antagonizing the transcriptional activity of beta-catenin. However, in this study, elevated TIP-1 expression levels were detected in human invasive breast cancers. Studies with two human invasive breast cancer cell lines indicated that RNAi-mediated TIP-1 knockdown suppressed the cell adhesion, proliferation, migration and invasion in vitro, and inhibited tumor growth in mammary fat pads and pulmonary metastasis in athymic mice. Biochemical studies showed that TIP-1 knockdown had moderate and differential effects on the beta-catenin-regulated gene expression, but remarkably down regulated the genes for cell adhesion and motility in breast cancer cells. The decreased expression of integrins and paxillin was accompanied with reduced cell adhesion and focal adhesion formation on fibronectin-coated surface. In conclusion, this study revealed a novel oncogenic function of TIP-1 suggesting that TIP-1 holds potential as a prognostic biomarker and a therapeutic target in the treatment of human invasive breast cancers.

AB - Tax-interacting protein 1 (TIP-1, also known as Tax1bp3) inhibited proliferation of colon cancer cells through antagonizing the transcriptional activity of beta-catenin. However, in this study, elevated TIP-1 expression levels were detected in human invasive breast cancers. Studies with two human invasive breast cancer cell lines indicated that RNAi-mediated TIP-1 knockdown suppressed the cell adhesion, proliferation, migration and invasion in vitro, and inhibited tumor growth in mammary fat pads and pulmonary metastasis in athymic mice. Biochemical studies showed that TIP-1 knockdown had moderate and differential effects on the beta-catenin-regulated gene expression, but remarkably down regulated the genes for cell adhesion and motility in breast cancer cells. The decreased expression of integrins and paxillin was accompanied with reduced cell adhesion and focal adhesion formation on fibronectin-coated surface. In conclusion, this study revealed a novel oncogenic function of TIP-1 suggesting that TIP-1 holds potential as a prognostic biomarker and a therapeutic target in the treatment of human invasive breast cancers.

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KW - Breast cancer

KW - Cell adhesion

KW - Migration

KW - Pulmonary metastasis

KW - Tax-interacting protein 1

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The PDZ protein TIP-1 facilitates cell migration and pulmonary metastasis of human invasive breast cancer cells in athymic mice

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