Ganglioside GD1a suppression of NOS2 expression via ERK1 pathway in mouse osteosarcoma FBJ cells

Ting Cao, Tianyi Zhang, Li Wang, Lan Zhang, Tomoko Adachi, Toshinori Sato, Sadako Yamagata, Tatsuya Yamagata

研究成果: Article

4 引用 (Scopus)

抜粋

Inducible nitric oxide synthase (NOS2) is over-expressed in a number of tumors and implicated in tumor growth and metastasis. Murine FBJ osteosarcoma-derived FBJ-S1 cells are poorly metastatic and express the ganglioside GD1a, whereas highly metastatic FBJ-LL cells only slightly express this ganglioside. The present study demonstrates that NOS2 is more highly expressed in FBJ-LL cells compared to FBJ-S1 cells. By manipulating GM2/GD2 synthase expression or adding exogenous GD1a, GD1a inversely regulated NOS2 at the transcriptional level. GT1b suppressed NOS2 to the same extent as GD1a. Silencing NOS2 inhibited proliferation, migration, and anchorage-independent growth of FBJLL cells, suggesting that the metastatic properties of FBJ-LL cells are associated with NOS2. MEK1/2 inhibitor (U0126) increased NOS2 expression, whereas GD1a treatment decreased it. Co-treating the cells with GD1a and U0126 blocked the inhibition of NOS2 expression, suggesting that the GD1a signal is mediated by ERK1/2. NOS2 expression increased when ERK1, but not ERK2, was silenced, and GD1a did not suppress NOS2 expression in cells treated with another MEK1/2 inhibitor PD98059, suggesting that ERK1 phosphorylation is indispensable for the GD1a signal suppressing NOS2.

元の言語English
ページ(範囲)1165-1174
ページ数10
ジャーナルJournal of Cellular Biochemistry
110
発行部数5
DOI
出版物ステータスPublished - 2010 8 1

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

フィンガープリント Ganglioside GD1a suppression of NOS2 expression via ERK1 pathway in mouse osteosarcoma FBJ cells' の研究トピックを掘り下げます。これらはともに一意のフィンガープリントを構成します。

  • これを引用