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Updated: Feb 23, 2026
Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies
Published on: July 3, 2025
Comprehensive DNA microarray expression profiles of tumors in tenascin-C-knockout mice
Kaori Matsumoto1, Yuji Nakai2, Masaru Hoshino3
1a Laboratory of Veterinary Surgery, Graduate School of Agricultural and Life Sciences , The University of Tokyo , Tokyo , Japan.
Abstract:
Tenascin-C (TNC), an extracellular matrix glycoprotein, plays a pivotal role in tumor growth. However, the mechanism whereby TNC affects tumor biology remains unclear. To investigate the exact role of TNC in primary tumor growth, a mouse mammary tumor cell line, GLMT1, was first developed. Subsequently, global gene expression in GLMT1-derived tumors was compared between wild-type (WT) and TNC-knockout (TNKO) mice. Tumors in WT mice were significantly larger than those in TNKO mice. DNA microarray analysis revealed 447 up and 667 downregulated in the tumors inoculated into TNKO mice as compared to tumors in WT mice. Validation by quantitative gene expression analysis showed that Tnc, Cxcl1, Cxcl2, and Cxcr2 were significantly upregulated in WT mice. We hypothesize that TNC stimulates the CXCL1/2-CXCR2 pathway involved in cancer cell proliferation.
Insights
Tenascin-C (TNC) promotes primary tumor growth by stimulating the CXCL1/2-CXCR2 pathway. Knocking out TNC significantly reduced tumor size, revealing TNC
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Tenascin-C (TNC) is an extracellular matrix glycoprotein implicated in tumor progression.
- The precise mechanisms by which TNC influences tumor biology are not fully understood.
Purpose of the Study:
- To elucidate the specific role of Tenascin-C (TNC) in primary tumor growth.
- To investigate the molecular pathways affected by TNC in mammary tumor development.
Main Methods:
- Development of a mouse mammary tumor cell line (GLMT1).
- Comparison of global gene expression in tumors from wild-type (WT) and TNC-knockout (TNKO) mice using DNA microarray.
- Validation of gene expression changes via quantitative analysis.
Main Results:
- Tumors in WT mice were significantly larger than those in TNKO mice.
- DNA microarray analysis identified numerous differentially expressed genes between WT and TNKO tumors.
- Quantitative analysis confirmed significant upregulation of Tnc, Cxcl1, Cxcl2, and Cxcr2 in WT mice.
Conclusions:
- Tenascin-C (TNC) significantly promotes primary mammary tumor growth.
- The TNC-mediated promotion of tumor growth is associated with the CXCL1/2-CXCR2 signaling pathway.
- This pathway is hypothesized to be involved in cancer cell proliferation.
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