ID1 controls aggressiveness of salivary gland cancer cells via crosstalk of IGF and AKT pathways

Tomoki Sumida, Yu Kamata, Yosuke Kobayashi, Akiko Ishikawa, Yoshihide Mori

研究成果: Contribution to journalArticle査読

3 被引用数 (Scopus)

抄録

Background: Inhibitor of differentiation or DNA binding 1 (ID1) is overexpressed in human salivary gland cancer (SGC). The insulin growth factor (IGF) system is an attractive target in cancer control because it is associated with various cancer progressions. Materials and Methods: The human SGC cell line HSY with abundant ID1 was used. ID1 knockdown and its effect on the IGF system were investigated. Cell proliferation and invasion, as well as associated protein expression, were analyzed. Phospho-AKT was also evaluated. Results: ID1 knockdown reduced cell proliferation and invasion, while the expression of proteins associated with malignant phenotypes was altered. IGF-II expression was suppressed, suggesting that this system is one of the mechanisms underlying effects of ID1 in SGC cells. c-Myc was up-regulated, whereas p21 and p27 were downregulated. Moreover, phospho-AKT was reduced in ID1-knockeddown cells. Conclusion: ID1 down-regulation induced parallel changes in the IGF and AKT pathways. The crosstalk of these pathways may enhance malignant phenotypes in SGCs.

本文言語英語
ページ(範囲)3865-3870
ページ数6
ジャーナルAnticancer research
36
8
出版ステータス出版済み - 8 2016

All Science Journal Classification (ASJC) codes

  • 腫瘍学
  • 癌研究

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