Abstract
Matrix metalloproteinases (MMPs) have been linked to the metastatic potential of tumor cells due to their ability to degrade the extracellular matrix. MMP-3 (stromelysin-1) is upregulated in a wide variety of human tumors. We used the MMTV-PyMT breast cancer model to determine if MMP-3 is involved in tumorigenesis and metastatic growth. In this model the stromal expression of MMP-3 mRNA resembles the predominant MMP-3 expression pattern observed in human ductal breast carcinomas. We studied a cohort of 63 PyMT transgenic mice, either deficient for MMP-3 or wild-type controls. The degree of metastasis did not differ significantly between the two groups of mice, although the median lung metastasis volume was more than threefold increased in MMTV-PyMT mice deficient in MMP-3. Likewise, primary tumor growth rate and lymph node metastasis were not significantly affected by MMP-3-deficiency. By comparing mRNA levels in MMP-3-deficient PyMT tumors with PyMT wild-type tumors we excluded compensatory transcriptional changes of other MMPs or their specific inhibitors. Thus, we conclude that genetic ablation of MMP-3 does not significantly affect tumor growth and metastasis in the MMTV-PyMT model.
| Original language | English |
|---|---|
| Journal | Molecular Carcinogenesis |
| Volume | 48 |
| Issue number | 7 |
| Pages (from-to) | 618-625 |
| Number of pages | 8 |
| ISSN | 0899-1987 |
| DOIs | |
| Publication status | Published - 2009 |
Keywords
- Animals
- Base Sequence
- DNA Primers
- Female
- Hydrolysis
- Male
- Matrix Metalloproteinase 3
- Mice
- Mice, Transgenic
- Neoplasm Metastasis
- Neoplasms, Experimental
- Polymerase Chain Reaction
- RNA, Messenger
