T47D breast cancer cell growth is inhibited by expression of VACM-1, a cul-5 gene
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Updated: Aug 24, 2026

Modeling Breast Cancer via an Intraductal Injection of Cre-expressing Adenovirus into the Mouse Mammary Gland
Published on: June 7, 2019
Maria A Burnatowska-Hledin1, Jennifer B Kossoris, Christa J Van Dort
1Department of Biology, Peale Science Center, Hope College, Holland, MI 49422-9000, USA. hledin@hope.edu
Abstract:
Vasopressin-activated calcium-mobilizing (VACM-1), a cul-5 gene, is localized on chromosome 11q22-23 close to the gene for Ataxia Telangiectasia in a region associated with a loss of heterozygosity in breast cancer tumor samples. To examine the biological role of VACM-1, we studied the effect of VACM-1 expression on cellular growth and gene expression in T47D breast cancer cells. Immunocytochemistry studies demonstrated that VACM-1 was expressed in 0.6-6% of the T47D cells and localized to the nucleus of mitotic cells. Overexpressing VACM-1 significantly attenuated cellular proliferation and MAPK phosphorylation when compared to the control cells. In addition, VACM-1 decreased egr-1 and increased Fas-L mRNA levels. Further, egr-1 protein levels were significantly lower in the nuclear fraction from VACM-1 transfected cells when compared to controls. These data indicate that VACM-1 is involved in the regulation of cellular growth.
Insights
Vasopressin-activated calcium-mobilizing (VACM-1) gene expression attenuated breast cancer cell proliferation and altered specific gene expression. VACM-1 plays a role in regulating cellular growth.
Area of Science:
- Molecular biology
- Genetics
- Cancer research
Background:
- Vasopressin-activated calcium-mobilizing (VACM-1) is a cul-5 gene located on chromosome 11q22-23.
- This chromosomal region shows loss of heterozygosity in breast cancer samples, suggesting a potential role in tumorigenesis.
Purpose of the Study:
- To investigate the biological role of VACM-1 in breast cancer.
- To examine the effects of VACM-1 expression on cellular growth and gene expression in T47D breast cancer cells.
Main Methods:
- Immunocytochemistry to determine VACM-1 expression and localization in T47D cells.
- Overexpression of VACM-1 in T47D cells.
- Analysis of cellular proliferation, MAPK phosphorylation, and mRNA levels of egr-1 and Fas-L.
- Western blot analysis of egr-1 protein levels in nuclear fractions.
Main Results:
- VACM-1 was detected in a small percentage of T47D cells, localizing to the nucleus of mitotic cells.
- Overexpression of VACM-1 significantly reduced cellular proliferation and MAPK phosphorylation.
- VACM-1 modulated gene expression by decreasing egr-1 mRNA and increasing Fas-L mRNA levels.
- Nuclear egr-1 protein levels were significantly lower in VACM-1 transfected cells.
Conclusions:
- VACM-1 expression is associated with reduced proliferation in T47D breast cancer cells.
- VACM-1 influences cellular growth regulation through modulation of specific gene expression, including egr-1 and Fas-L.
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