A multifaceted role for Myd88-dependent signaling in progression of murine mammary carcinoma

Previous data obtained in our laboratory suggested that there may be constitutive signaling through the myeloid differentiation primary response gene 88 (Myd88)-dependent signaling cascade in murine mammary carcinoma. Here, we extended these findings by showing that, in the absence of an added Toll-like receptor (TLR) agonist, the myddosome complex was preformed in 4T1 tumor cells, and that Myd88 influenced cytoplasmic extracellular signal–regulated kinase (Erk)1/Erk2 levels, nuclear levels of nuclear factor-kappaB (NFκB) and signal transducer and activator of transcription 5 (STAT5), tumor-derived chemokine (C–C motif) ligand 2 (CCL2) expression, and in vitro and in vivo tumor growth. In addition, RNA-sequencing revealed that Myd88-dependent signaling enhanced the expression of genes that could contribute to breast cancer progression and genes previously associated with poor outcome for patients with breast cancer, in addition to suppressing the expression of genes capable of inhibiting breast cancer progression. Yet, Myd88-dependent signaling in tumor cells also suppressed expression of genes that could contribute to tumor progression. Collectively, these data revealed a multifaceted role for Myd88-dependent signaling in murine mammary carcinoma.

Title	A multifaceted role for Myd88-dependent signaling in progression of murine mammary carcinoma
Creator	Boateng, K. Y.
	Parsons, V. A.
	Eidelman, A. S.
	Ricca, J. M.
	Seifert, A.
	Phoung, T.
	Carey, M. A.
	Higgins, M. J.
	Kurt, Robert A.
	Tucker, K. C.
	Serrano, A.
Publisher	Breast Cancer: Basic and Clinical Research
Academic Department	Biology
Division	Natural Sciences
Organization	Lafayette College
Date Issued	October 2016
Date Available	2016-11-08T15:32:18Z
Type	Article
Language	English
Keyword	NFκB
	4T1
	beast cancer
	Myd88
	RNA-Seq
Bibliographic Citation	Higgins, M. J., et al. (2016 Oct) "A multifaceted role for Myd88-dependent signaling in progression of murine mammary carcinoma." Breast Cancer: Basic and Clinical Research 10: 157-67.
Standard Identifier	DOI 10.4137/BCBCR.S40075
Standard Identifier	Handle 10385/2154
Permalink	http://hdl.handle.net/10385/2154
Rights Statement	Creative Commons - Attribution, Non-Commercial
Rights Holders	Tucker, K. C.
	Parsons, V. A.
	Eidelman, A. S.
	Libertas Academica Limited
	Ricca, J. M.
	Seifert, A.
	Phoung, T.
	Serrano, A.
	Higgins, M. J.
	Kurt, Robert A.
	Boateng, K. Y.
	Carey, M. A.