Taken together, our data indicate that loss of AAMP from NSCLC inhibits tumor growth and elevates drug sensitivity, and these findings have clinical implications to treat NSCLC cancers.
According to our findings, AAMP knockdown inhibited lung cancer cell proliferation and inhibited lung cancer cell tumorigenesis in the mouse xenograft model.
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 has a significant influence on the biological functions of breast cancer cells and its high expression correlates with poor prognosis and metastasis.
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.
Further study of angio-associated migratory cell protein by quantitative reverse transcriptase-PCR and in situ hybridization analysis of 37 cases of DCIS confirmed higher mRNA expression in DCIS(necrosis+) (P = 0.0095).
Upon analysis of the tissue distribution of AAMP, it was found to be expressed strongly in endothelial cells, cytotrophoblasts, and poorly differentiated colon adenocarcinoma cells found in lymphatics.