Growth, metastasis, and expression of CCL2 and CCL5 by murine mammary carcinomas are dependent upon Myd88

Previously we reported that lipopolysaccharide (LPS) treatment of murine mammary carcinomas resulted in decreased growth of the tumors. Here we show the decreased growth following LPS treatment was mediated through effects downstream of TLR4 and Myd88. Perhaps more notably, simply reducing TLR4 or Myd88 levels was sufficient to slow tumor growth rates. Moreover, reduced levels of Myd88 correlated with a significant reduction in lung metastasis as well as decreased CCL2 and CCL5 expression. To determine whether inhibiting Myd88 function could also alter tumor growth and chemokine expression we used a Myd88 homodimerization inhibitory peptide. Indeed, inhibiting Myd88 function in four different murine mammary carcinomas as well as the human breast cancer cell line MDA-MB-231 led to decreased growth as well as CCL2 and CCL5 expression. These data imply that Myd88 is important for growth and metastasis of breast cancer, and expression of at least two proinflammatory chemokines.

Title	Growth, metastasis, and expression of CCL2 and CCL5 by murine mammary carcinomas are dependent upon Myd88
Creator	Ewer, J. C.
	Egunsola, A. T.
	Chalmers, S. A.
	Akuffo, A. A.
	Perez, D. N.
	Lombardo, J. C.
	Vail, C. M.
	Zawislak, C. L.
	Kurt, Robert A.
Publisher	Cellular Immunology
Academic Department	Biology
Division	Natural Sciences
Organization	Lafayette College
Date Issued	2012
Date Available	2015-06-05T18:47:00Z
Type	Article
Language	English
Keyword	4T1
	breast cancer
	metastasis
	MDA-MB-231
	Myd88
	TLR
Bibliographic Citation	Egunsola, A. T., et al. (2012) "Growth, metastasis, and expression of CCL2 and CCL5 by murine mammary carcinomas are dependent upon Myd88." Cellular Immunology 272 (2): 220-229.
Standard Identifier	Handle 10385/1989
Standard Identifier	DOI 10.1016/j.cellimm.2011.10.008
Permalink	http://hdl.handle.net/10385/1989
Rights Statement	In Copyright
Rights Holders	Elsevier Inc.