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Scanning electron microscopy with an ionic liquid reveals the loss of mitotic protrusions of cells during the epithelial–mesenchymal transition
Author(s) -
Ishigaki Yasuhito,
Nakamura Yuka,
Takehara Teruaki,
Shimasaki Takeo,
Tatsuno Takanori,
Takano Fumihide,
Ueda Yoshimichi,
Motoo Yoshiharu,
Takegami Tsutomu,
Nakagawa Hideaki,
Kuwabata Susumu,
Nemoto Noriko,
Tomosugi Naohisa,
Miyazawa Shichiro
Publication year - 2011
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/jemt.20989
Subject(s) - filopodia , microbiology and biotechnology , vimentin , epithelial–mesenchymal transition , mitosis , mesenchymal stem cell , cell , chemistry , pseudopodia , cell growth , biology , downregulation and upregulation , actin , immunology , biochemistry , immunohistochemistry , gene
Epithelial–mesenchymal transition (EMT) is a key event in cancer metastasis and is characterized by increase in cell motility, increase in expression of mesenchymal cell markers, loss of proteins from cell‐to‐cell junction complexes, and changes in cell morphology. Here, the morphological effects of a representative EMT inducer, transforming growth factor (TGF)‐β1, were investigated in human lung adenocarcinoma (A549) cells and pancreatic carcinoma (Panc‐1) cells. TGF‐β1 caused morphological changes characteristic of EMT, and immunostaining showed loss of E‐cadherin from cell‐to‐cell junction complexes in addition to the upregulation of the mesenchymal marker vimentin. During scanning electron microscopy (SEM) with an ionic liquid, we observed EMT‐specific morphological changes, including the formation of various cell protrusions. Interestingly, filopodia in mitotic cells were clearly observed by SEM, and the number of these filopodia in TFG‐β1‐treated mitotic cells was reduced significantly. We conclude that this reduction in such mitotic protrusions is a novel effect of TGF‐β1 and may contribute to EMT. Microsc. Res. Tech., 2011. © 2011 Wiley Periodicals, Inc.