alexa The impact of angio-associated migratory cell protein (AAMP) on breast cancer cells in vitro and its clinical significance


Angiology: Open Access

Author(s): Yin Y

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Angio-associated migratory cell protein (AAMP), which belongs to the immunoglobulin superfamily, was found to be expressed in different human cell lines and exhibited a predominant cytosolic localization in epithelial cells. Previous studies show that the specific gene product is functional in cell migration and angiogenesis and can also be used as a marker of poor prognosis in invasive gastrointestinal stromal tumours and ductal carcinoma in situ (DCIS) of the breast. However, the cellular role of AAMP in breast cancer is still unclear. The aim of the current study was to provide new insights into the implication of AAMP in breast cancer.


We knocked-down the expression of AAMP through transfection of MCF-7 and MDA-MB-231 breast cancer cells with a hammerhead ribozyme transgene (MCF-7(AAMPrib) and MDA-MB-231(AAMPrib)) and examined the impact on cell function using in vitro assays. Additionally, AAMP expression was examined in a cohort of breast specimens (normal, n=28; cancer, n=102) using quantitative-real-time polymerase chain reaction (Q-PCR) and immunohistochemical methods.


AAMP knock-down dramatically reduced cell adhesion and cell growth of MCF-7 cells (p<0.05), and suppressed cell invasion of MDA-MB-231 cells (p<0.05). Increased expression of AAMP in breast cancer was observed compared with that in normal tissues (p<0.05). High levels of AAMP transcripts were associated with disease progression, metastasis, and poor prognosis of the patients. Disease-free and overall survival time of patients with lower levels of AAMP were significantly longer compared to those of patients with high levels (p<0.05).


AAMP has a significant influence on the biological functions of breast cancer cells and its high expression correlates with poor prognosis and metastasis.

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This article was published in Anticancer Res and referenced in Angiology: Open Access

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