Lymph node-positive breast cancers have a poor cell progression and worse prognosis that is manifested by distant metastases with short survival than node-negative cases. However, the intrinsic nature of gene dysregulation, triggering tumor cells to metastasize remains to be an issue of extraordinarily inextricable complexity. To address the functional consequences of differential expression of metastasis-associated protein 1 (MTA1), cyclin D1 and β-catenin in breast cancer with axillary lymph node metastasis (LNM), forty-six breast cancer patients enrolled, including 27 cancer tissues manifesting lymph node metastasis examined by HE staining on lymph nodes. The mRNA expression was examined in breast tumor and paired adjacent normal tissues which were collected and evaluated by quantitative reverse transcription polymerase chain reaction (qRT- PCR). The expression level of each cancer patient was defined as tumor/normal ratios based on internal positive control of β-actin gene. Increased expression of MTA1 gene in breast cancer with LNM was found as compared to breast cancer without LNM, and which reached statistically significant (p=0.0174). On the other hand, either cyclin D1 or β-catenin expression was not significantly associated with breast cancer patients with LNM in univariate analysis (p=0.244 for cyclin D1 and p=0.142 for β-catenin, respectively). With regard to the status of estrogen receptor (ER) positive, the elevated risk in breast cancer having LNM was associated in patient with high expression of MTA1 gene (OR=1.525; 95%CIs=1.077-2.159). In addition, as to cases showing ER-positive, the higher level of cyclin D1 expression was observed in poorly differentiated breast cancer than that in well differentiated breast cancer, and which result was borderline significant (OR=1.318; 95%CIs=0.934-1.859). The present study provides evidences that up-regulated expression of MTA1 gene can be regarded as a marker in the prediction of breast cancer patients with the phenotype of lymph node metastasis.

[Proc Amer Assoc Cancer Res, Volume 46, 2005]