In previous research, BP1 appears to be associated with metastasis, shown by immunostaining on 46 samples of inflammatory breast cancer (as well as matched lymph nodes in 9 metastatic cases); all cases were BP1 positive. Now we suggest that BP1 induces breast cancer cells to undergo the epithelial to mesenchymal like transition (EMT). EMT, a process in which cancer cells lose their epithelial features and gain mesenchymal markers, enables tumor cells to become more invasive and migratory, and can lead to metastasis. BP1 upregulate Twist, a basic helix-loop-helix (bHLH) transcription factor which triggers EMT. Twist is well known for initiation of EMT in various cancers. We found that BP1 can upregulate Twist expression in two breast cancer cell lines, MCF-7 and HS578T, and induce EMT, resulting in increased migratory ability. On the other hand, exogenous BP1 can also increase Twist expression and migration ability of cancer cell lines, indicating that BP1 might be able to induce EMT in both a paracrine and endogenous manner.
|Advisor:||Berg, Patricia E.|
|School:||The George Washington University|
|Department:||Biochemistry and Molecular Biology|
|School Location:||United States -- District of Columbia|
|Source:||MAI 49/01M, Masters Abstracts International|
|Subjects:||Molecular biology, Cellular biology|
|Keywords:||Breast cancer, Epithelial to mesenchymal transition, Homeobox genes, Metastasis|
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