{'fraction_non_alphanumeric': 0.04656862745098039, 'fraction_numerical': 0.0032679738562091504, 'mean_word_length': 5.621621621621622, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
A complex containing LPP and &agr;-actinin mediates TGF&bgr;-induced migration and invasion of ErbB2-expressing breast cancer cells

Summary Transforming growth factor &bgr; (TGF&bgr;) is a potent modifier of the malignant phenotype in ErbB2-expressing breast cancers. We demonstrate that epithelial-derived breast cancer cells, which undergo a TGF&bgr;-induced epithelial-to-mesenchymal transition (EMT), engage signaling molecules that normally facilitate cellular migration and invasion of mesenchymal cells. We identify lipoma preferred partner (LPP) as an indispensable regulator of TGF&bgr;-induced migration and invasion of ErbB2-expressing breast cancer cells. We show that LPP re-localizes to focal adhesion complexes upon TGF&bgr; stimulation and is a critical determinant in TGF&bgr;-mediated focal adhesion turnover. Finally, we have determined that the interaction between LPP and &agr;-actinin, an actin cross-linking protein, is necessary for TGF&bgr;-induced migration and invasion of ErbB2-expressing breast cancer cells. Thus, our data reveal that LPP, which is normally operative in cells of mesenchymal origin, can be co-opted by breast cancer cells during an EMT to promote their migration and invasion.