{'fraction_non_alphanumeric': 0.03902439024390244, 'fraction_numerical': 0.03121951219512195, 'mean_word_length': 4.7, '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 interaction of TGF-β-Smads/miR-362-3p/CD82 mediated by M2 macrophages promotes the process of EMT in HCC cells.

Abnormal tumor microenvironment and the epithelial-mesenchymal transition (EMT) are important features of tumor metastasis. However, it remains unknown how signals can form complicated networks to regulate the sustainability of the EMT process. The aim of our study is to explore the possible interaction between tumor-associated macrophages (TAMs) and tumor cells in the EMT process mediated by miR-362-3p. In this study, we found that by releasing TGF-β, M2 macrophages mediate binding of Smad2/3 to miR-362-3p promoter, leading to overexpression of miR-362-3p. miR-362-3p maintains EMT by regulating CD82, one of the most important members of tetraspanins. Our findings suggests that miR-362-3p can serve as a core factor mediating crosstalk between the TGF-β pathway in TAMs and tetraspanins in tumor cells, and thus facilitates the EMT process. This article is protected by copyright. All rights reserved.