Association between Expression of Tissue Inhibitors of Metalloproteinases‑1, Matrix Metalloproteinase‑2, and Matrix Metalloproteinase‑9 Genes and Axillary Lymph Nodes Metastasis in Patients with Breast Cancer

Alireza Abdollahi, Zohreh Nozarian, Elham Nazar


Background: Certain enzymatic biomarkers such as matrix metalloproteinase (MMPs) are instrumental in the breast cancer. Hence, they are viewed as predictive biomarkers in the primary prognosis of this type of cancer. Furthermore, they enjoy a predictive value in the evaluation of the disease, recurrence of tumor, invasion of tumor cells to other areas as well as therapeutic outcomes. The present study aimed to determine the association between the expression of the three tissue
inhibitors of metalloproteinases‑1 (TIMP1), MMP2, and MMP9 genes and axillary lymph nodes involvement in patients with breast cancer.

Methods: Patients in this study were categorized into two groups, frst with axillary lymph nodes involvement (as the case group) and second group without the involvement of axillary lymph nodes (as the control group) referred to Cancer Institute at Imam Khomeini Hospital in Tehran in 2016. The gene expression was assessed using the reverse transcription polymerase‑chain reaction technique.

Results: There was no signifcant difference in the mRNA level of MMP2 and MMP9 genes between the cancer tissues with and without axillary lymph node metastasis in comparison with normal samples. However, the mRNA level of TIMP1
gene was considerably higher in the cancer tissue with axillary lymph node metastasis as compared to the samples without metastasis. In other words, the presence of axillary lymph node metastasis induced a 77.8‑fold increase in mRNA expression when compared to condition without metastasis.

Conclusions: The expression of TIMP1 gene is strongly associated with axillary lymph node metastasis in breast cancer patients.

Keywords: Breast cancer, lymph nodes, matrix metalloproteinase‑2, matrix metalloproteinase‑9, tissue inhibitors of metalloproteinases‑1

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