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Targeting ID2 expression triggers a more differentiated phenotype and reduces aggressiveness in human salivary gland cancer cells
Author(s) -
Sumida Tomoki,
Ishikawa Akiko,
Nakano Hiroyuki,
Yamada Tomohiro,
Mori Yoshihide,
Desprez PierreYves
Publication year - 2016
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/gtc.12389
Subject(s) - gene knockdown , biology , vimentin , transcription factor , phenotype , cadherin , microbiology and biotechnology , cellular differentiation , cell growth , cancer research , cell , cell culture , immunology , genetics , gene , immunohistochemistry
Inhibitors of DNA‐binding (ID) proteins are negative regulators of basic helix‐loop‐helix transcription factors and generally stimulate cell proliferation and inhibit differentiation. We previously determined that ID1 was highly expressed in aggressive salivary gland cancer (SGC) cells in culture. Here, we show that ID2 is also expressed in aggressive SGC cells. ID2 knockdown triggers important changes in cell behavior, that is , it significantly reduces the expression of N‐cadherin, vimentin and Snail, induces E‐cadherin expression and leads to a more differentiated phenotype exemplified by changes in cell shape. Moreover, ID2 knockdown almost completely suppresses invasion and the expression of matrix metalloproteinase 9. In conclusion, ID2 expression maintains an aggressive phenotype in SGC cells, and ID2 repression triggers a reduction in cell aggressiveness. ID2 therefore represents a potential therapeutic target during SGC progression. ID proteins are negative regulators of basic helix‐loop‐helix transcription factors and generally stimulate cell proliferation and inhibit differentiation. ID2 knockdown triggers important changes in cell behavior, that is, it significantly reduces the expression of N‐cadherin, vimentin and Snail, induces E‐cadherin expression and leads to a more differentiated phenotype exemplified by changes in cell shape. ID2 therefore represents a potential therapeutic target during SGC progression.