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Updated: Jun 24, 2026
09:01
Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies
Published on: July 3, 2025
PRIP promotes tumor formation through enhancing serum-responsive factor-mediated FOS expression
Yiwei Tony Zhu1, Liping Hu, Chao Qi
1Department of Pathology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois 60611, USA.
The Journal of Biological Chemistry
|March 31, 2009
Summary
Peroxisome proliferator-activator receptor interacting protein (PRIP) deficiency inhibits breast tumor formation by reducing FOS gene expression and cell invasion. Restoring FOS expression reverses these effects, highlighting PRIP
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Biology
Background:
- Peroxisome proliferator-activator receptor interacting protein (PRIP) is a nuclear receptor coactivator crucial for mammary gland development.
- The role of PRIP in breast tumorigenesis remains incompletely understood.
Purpose of the Study:
- To investigate the function of PRIP in breast cancer development and progression.
- To elucidate the molecular mechanisms by which PRIP influences tumor formation and metastasis.
Main Methods:
- Establishment of a mammary tumor cell line with conditional PRIP gene knockout (PRIP(Loxp/Loxp)).
- Assessment of tumor formation, cell proliferation, invasion, and migration following PRIP gene deletion.
- Chromatin immunoprecipitation (ChIP) assays to determine PRIP recruitment to the FOS promoter.
- Analysis of FOS gene expression regulation by PRIP in human breast cancer cells.
- Re-expression of FOS in PRIP-deficient cells to confirm its role in tumor formation.
Main Results:
- PRIP deficiency in mammary tumor cells inhibited tumor formation without affecting proliferation.
- PRIP knockout led to decreased cell invasion and migration capabilities.
- PRIP deficiency substantially reduced FOS gene expression, and PRIP was recruited to the FOS promoter.
- PRIP directly up-regulated FOS gene expression in human breast cancer cells, acting through serum-responsive factor.
- Re-expression of FOS confirmed that reduced FOS expression mediated the inhibited tumor formation in PRIP-deficient cells.
Conclusions:
- PRIP plays a significant role in promoting breast tumor formation and metastasis.
- PRIP regulates FOS gene expression, which is critical for its oncogenic function in breast cancer.
- Targeting PRIP or its downstream effector FOS may represent a therapeutic strategy for breast cancer.
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