{'fraction_non_alphanumeric': 0.02531645569620253, 'fraction_numerical': 0.0, 'mean_word_length': 5.362068965517241, '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}}
E-cadherin interacts with EGFR resulting in hyper-activation of ERK in multiple models of breast cancer

The loss of the intercellular adhesion molecule E-cadherin is a hallmark of the epithelial- mesenchymal transition (EMT), during which tumor cells transition into an invasive phenotype. Accordingly, E-cadherin has long been considered a tumor suppressor gene. Using novel multi-compartment spheroids and multiple in vivo models, we show that E-cadherin promotes a hyper-proliferative phenotype in breast cancer cells via interaction with the transmembrane receptor EGFR. This interaction results in the activation of the MEK/ERK signaling pathway, leading to a significant increase in proliferation via the activation of transcription factors including c-Fos. Pharmacological inhibition of MEK activity in E-cadherin positive breast cancer cells significantly decreases both tumor growth and macro-metastasis in vivo. This work provides evidence for a novel role of E-cadherin in breast tumor growth and identifies a potential new target to treat hyper-proliferative E-cadherin-positive breast tumors.