Related Experiment Video
Updated: Apr 26, 2026

Comparative Lesions Analysis Through a Targeted Sequencing Approach
Published on: November 5, 2019
Comparative expression of matrix metalloproteinases in internal malignancies and paired cutaneous metastatic lesions
Tae Hyung Kim1, Jin Young Jung, Hyo Jin Roh
1*Department of Dermatology, Gangnam Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; †Yeouido Oracle Cosmetic Dermatosurgery Clinic, Seoul, Korea; and ‡Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Background:
Matrix metalloproteinase (MMP), tissue inhibitor of metalloproteinase (TIMP), and membrane-type 1 matrix metalloproteinase (MT1-MMP) are thought to be involved in the destruction of basement membrane and stromal invasion by cancer cells.
Objective:
The aim of this study was to identify and compare MMP and TIMP expression in internal malignancies and paired cutaneous metastatic lesions.
Materials And Methods:
We compared the expression of MMP-2, MMP-9, MT1-MMP, and TIMP-2 in the internal malignancy and paired cutaneous metastatic lesion using immunohistochemical stains.
Results:
The cutaneous metastatic lesions expressed significantly more MMP-2, MMP-9, and MT1-MMP and significantly less TIMP-2 than did the paired internal malignancies. In breast cancer, cutaneous metastatic lesions expressed significantly more MMP-9 and significantly less TIMP-2 than did the primary breast cancer lesion. In lung cancer, the cutaneous metastatic lesion expressed significantly more MMP-2 and MT1-MMP than did the primary lesion. In stomach cancer, the cutaneous metastatic lesion expressed significantly less TIMP-2 than did the primary lesion.
Conclusions:
Our study demonstrates that cutaneous metastatic lesions have different MMPs and TIMP-2 expression patterns compared with their paired internal malignancies. Also, MMPs and TIMP-2 expression differs according to the type of primary cancer.
Insights
Cutaneous metastatic lesions show altered expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) compared to primary tumors. These molecular differences in MMPs and TIMPs vary by cancer type.
Area of Science:
- Oncology
- Cancer Metastasis
- Molecular Biology
Background:
- Matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), and membrane-type 1 matrix metalloproteinase (MT1-MMP) are implicated in cancer cell invasion.
- These enzymes play a role in basement membrane degradation and stromal invasion during metastasis.
Purpose of the Study:
- To identify and compare the expression of MMPs and TIMPs in internal malignancies and their corresponding cutaneous metastatic lesions.
- To investigate differences in MMP-2, MMP-9, MT1-MMP, and TIMP-2 expression between primary cancers and skin metastases.
Main Methods:
- Immunohistochemical staining was employed to compare the expression levels of specific MMPs and TIMP-2.
- Expression patterns were analyzed in paired samples of internal malignancies and cutaneous metastatic lesions.
- Specific analyses were conducted for breast, lung, and stomach cancers.
Main Results:
- Cutaneous metastatic lesions exhibited significantly higher expression of MMP-2, MMP-9, and MT1-MMP, and lower expression of TIMP-2 compared to paired internal malignancies.
- In breast cancer, metastatic lesions showed increased MMP-9 and decreased TIMP-2.
- Lung cancer metastases had elevated MMP-2 and MT1-MMP, while stomach cancer metastases displayed reduced TIMP-2.
Conclusions:
- Cutaneous metastatic lesions display distinct MMP and TIMP-2 expression profiles compared to their primary internal tumors.
- The expression patterns of MMPs and TIMP-2 are influenced by the primary cancer type, suggesting tissue-specific metastatic behavior.
Related Concept Videos
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Role of Matrix Metalloproteases in Degradation of ECM
The Tumor Microenvironment

