Polypeptide N-acetylgalactosaminyltransferase 6 disrupts mammary acinar morphogenesis through O-glycosylation of fibronectin

JH Park, T Katagiri, S Chung, K Kijima, Y Nakamura - Neoplasia, 2011 - Elsevier
Neoplasia, 2011Elsevier
A high expression of short and immature O-glycans is one of the prominent features of
breast cancer cells, which would be attributed to the upregulated expression of
glycosyltransferases. Therefore, a detailed elucidation of glycosyltransferases and their
substrate (s) may improve our understandings for their roles in mammary carcinogenesis.
Here we report that overexpression of polypeptide N-acetylgalactosaminyltransferase 6
(GALNT6), a glycosyltransferase involved in the initial step of O-glycosylation, has …
Abstract
A high expression of short and immature O-glycans is one of the prominent features of breast cancer cells, which would be attributed to the upregulated expression of glycosyltransferases. Therefore, a detailed elucidation of glycosyltransferases and their substrate(s) may improve our understandings for their roles in mammary carcinogenesis. Here we report that overexpression of polypeptide N-acetylgalactosaminyltransferase 6 (GALNT6), a glycosyltransferase involved in the initial step of O-glycosylation, has transformational potentials through disruptive acinar morphogenesis and cellular changes similar to epithelial-to-mesenchymal transition in normal mammary epithelial cell, MCF10A. As one of the critical O-glycan substrates, we identified fibronectin that was O-glycosylated in vivo and thereby stabilized by GALNT6. Because knockdown of fibronectin abrogated the disruptive proliferation caused by introduction of GALNT6 into epithelial cells, our findings suggest that GALNT6-fibronectin pathway should be a critical component for breast cancer development and progression.
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