A Multifaceted Role for Myd88-Dependent Signaling in Progression of Murine Mammary Carcinoma

Breast Cancer: Basic and Clinical Research

Original Research

Kofi Y. Boateng¹  Antonio Serrano¹  Kyle C. Tucker¹  Maureen A. Carey¹  Robert A. Kurt¹  Mary J. Higgins¹  Tiffany Phuong¹  Jacob M. Ricca¹  Alec S. Eidelman¹  Alyssa Seifert¹  Victoria A. Parsons¹ 

[1] Department of Biology, Lafayette College, Easton, PA, USA.;

关键词: breast cancer;    4T1;    Myd88;    NFκB;    RNA-Seq;   

DOI  :  10.4137/BCBCR.S40075

 received in 2016-05-04, accepted in 2016-07-12,  发布年份 2016

来源: Sage Journals

【 摘 要 】

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.

【 授权许可】

CC BY-NC   
© 2016 SAGE Publications.

【 图 表 】

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