Open AccessNod1-dependent control of tumor growth
Author(s) -
Jean da Silva Correia,
Yvonne Miranda,
Nikki Austin-Brown,
Jenny Hsu,
John C. Mathison,
Rong Xiang,
Hongyu Zhou,
Qinxi Li,
Jiahuai Han,
Richard J. Ulevitch
Publication year - 2006
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.0509228103
Subject(s) - estrogen , peptidoglycan , nod1 , cell growth , biology , in vitro , microbiology and biotechnology , cell culture , growth inhibition , cytosol , cancer research , immune system , chemistry , immunology , endocrinology , biochemistry , enzyme , innate immune system , genetics , nod2
Nod1, a cytosolic protein that senses meso-diaminopimelic acid-containing ligands derived from peptidoglycan, plays a role in host responses to invasive bacteria. Here we describe a function for Nod1, whereby it controls tumor formation. Cell lines derived from the human breast cancer epithelial cell line MCF-7 were used in a severe combined immune deficiency (SCID) mouse xenograft model to characterize a pathway linking Nod1 to the growth of estrogen-sensitive tumors. In MCF-7 cells, the absence of Nod1 correlates with tumor growth, an increased sensitivity to estrogen-induced cell proliferation, and a failure to undergo Nod1-dependent apoptosis. Conversely, overexpression of Nod1 in MCF-7 cells results in inhibition of estrogen-dependent tumor growth and reduction of estrogen-induced proliferative responses in vitro.