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Updated: May 1, 2026
Experimental Metastasis Assay
Published on: August 24, 2010
B‑cell translocation 1 gene inhibits cellular metastasis‑associated behavior in breast cancer
Wei Li1, Shi-Tao Zou2, Ran Zhu3
1Department of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China.
Abstract:
B-cell translocation gene 1 (BTG1) is a member of the BTG/transducer of ERBB2 family, which regulates cell cycle progression in a variety of cell types and may have a role in inhibiting proliferation, promoting apoptosis and stimulating cellular differentiation in numerous cell types. However, the role of BTG1 in cancer metastasis is yet to be elucidated. In the present study, analysis of clinical specimens revealed that BTG1 mRNA levels were lower in lymph node metastases than those in benign breast tumors and normal human breast tissue. The effect of BTG1 on the metastatic behavior of breast cancer cells following stable transfection with a BTG1 expression vector was also investigated. The overexpression of BTG1 was observed to inhibit cell adhesion, migration and invasion. Furthermore, the overexpression of BTG1 was found to be involved in the inhibition of the metastasis-related proteins matrix metalloproteinase-2 and -9, as well as the promotion of the cell-cell adhesion-associated protein E-cadherin. In syngeneic nude mice breast tumor models, hepatic metastasis and angiogenesis were observed in the mice injected with the control cells, but not in those injected with pcDNA3-BTG1 cells. Immunohistochemistry revealed that overexpression of BTG1 decreased vascular endothelial growth factor expression in tumors. To the best of our knowledge, this is the first study to show that BTG1 overexpression decreases migration and invasion of breast cancer cells and thereby inhibits distant metastasis in mice breast tumor models.
Insights
B-cell translocation gene 1 (BTG1) is downregulated in breast cancer metastasis. Overexpressing BTG1 inhibits cancer cell migration, invasion, and metastasis in preclinical models, suggesting a tumor-suppressive role.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- B-cell translocation gene 1 (BTG1) is part of the BTG/transducer of ERBB2 family, known to regulate cell cycle progression.
- BTG1's role in cancer metastasis, particularly in breast cancer, remains largely uncharacterized.
- Previous studies suggest BTG1 may inhibit proliferation and promote apoptosis and differentiation.
Purpose of the Study:
- To investigate the role of BTG1 in breast cancer metastasis.
- To analyze BTG1 expression levels in clinical breast tumor specimens.
- To evaluate the impact of BTG1 overexpression on breast cancer cell metastatic behavior in vitro and in vivo.
Main Methods:
- Analysis of BTG1 mRNA levels in clinical breast tumor tissues and lymph node metastases.
- Stable transfection of breast cancer cells with a BTG1 expression vector.
- In vitro assays assessing cell adhesion, migration, and invasion.
- Western blot analysis of metastasis-related proteins (MMP-2, MMP-9, E-cadherin).
- In vivo studies using syngeneic nude mice breast tumor models to assess metastasis and angiogenesis.
- Immunohistochemistry to evaluate vascular endothelial growth factor (VEGF) expression.
Main Results:
- BTG1 mRNA levels were significantly lower in lymph node metastases compared to benign tumors and normal breast tissue.
- Overexpression of BTG1 in breast cancer cells inhibited cell adhesion, migration, and invasion.
- BTG1 overexpression reduced levels of metastasis-promoting proteins (MMP-2, MMP-9) and increased cell-cell adhesion protein (E-cadherin).
- In vivo, BTG1 overexpression suppressed hepatic metastasis and angiogenesis in mouse models.
- Tumor VEGF expression was decreased by BTG1 overexpression.
Conclusions:
- BTG1 expression is reduced in metastatic breast cancer tissues.
- BTG1 functions as a suppressor of breast cancer cell migration, invasion, and metastasis.
- BTG1 overexpression inhibits key metastasis-related proteins and angiogenesis, offering a potential therapeutic target for reducing breast cancer spread.
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