A role for HMGB1, HSP60 and Myd88 in growth of murine mammary carcinoma in vitro

Previously we reported that Myd88 contributed to tumor progression. To begin to decipher what may be inducing Myd88 dependent signaling we focused on proteins that could function as damage associated molecular pattern molecules (DAMPs) since DAMPs have been reported to be secreted by tumors, and certain DAMPs mediate effects through toll-like receptors. A screen of mammary carcinoma for DAMP expression showed HMGB1 and HSP60 were significantly elevated relative to normal mammary epithelium, and targeting these DAMPs, or receptors for these DAMPs influenced growth of tumor cells. Moreover, analysis using a Myd88 inhibitory peptide suggested that HMGB1 mediated its effects in a Myd88 dependent manner, and inhibiting Myd88 function decreased HMGB1 and HSP60 gene expression. Collectively, these data suggest that HMGB1 and HSP60 contribute to growth of mammary carcinoma cells, HMGB1 accomplishes this, at least in part, through Myd88 dependent signaling, and these DAMPs are expressed in a Myd88 dependent manner.

Title	A role for HMGB1, HSP60 and Myd88 in growth of murine mammary carcinoma in vitro
Creator	Ewer, J. C.
	Eidelman, A. S.
	Chalmers, S. A.
	Ricca, J. M.
	Serrano, A.
	Vail, C. M.
	Kurt, Robert A.
	Tucker, K. C.
Publisher	Cellular Immunology
Academic Department	Biology
Division	Natural Sciences
Organization	Lafayette College
Date Issued	2013
Date Available	2015-06-05T18:27:12Z
Type	Article
Language	English
Keyword	HSP60
	4T1
	HMGB1
	breast cancer
	Myd88
Bibliographic Citation	Chalmers, S. A., et al. (2013) "A role for HMGB1, HSP60 and Myd88 in growth of murine mammary carcinoma in vitro." Cellular Immunology 282 (2): 136–145.
Standard Identifier	Handle 10385/1987
Standard Identifier	DOI 10.1016/j.cellimm.2013.04.014
Permalink	http://hdl.handle.net/10385/1987
Rights Statement	In Copyright
Rights Holders	Elsevier