RT Journal Article SR Electronic T1 Serum amyloid alpha 1-2 are not required for systemic inflammation in the 4T1 murine breast cancer model JF bioRxiv FD Cold Spring Harbor Laboratory SP 2022.09.26.509617 DO 10.1101/2022.09.26.509617 A1 He, Chenfeng A1 Konishi, Riyo A1 Harata, Ayano A1 Nakamura, Yuki A1 Mizuno, Rin A1 Yoda, Mayuko A1 Toi, Masakazu A1 Kawaguchi, Kosuke A1 Kawaoka, Shinpei YR 2022 UL http://biorxiv.org/content/early/2022/09/28/2022.09.26.509617.abstract AB Cancers induce the production of acute phase proteins such as serum amyloid alpha (SAA) in the liver and cause systemic inflammation. Despite the well-known coincidence of acute phase response and systemic inflammation, the direct roles of SAA proteins in systemic inflammation in the cancer context remains incompletely characterized, particularly in vivo. Here, we investigate the in vivo significance of SAA proteins in systemic inflammation in the 4T1 murine breast cancer model. 4T1 cancers elevate the expression of SAA1 and SAA2, the two major murine acute phase proteins in the liver. The elevation of Saa1-2 correlates with the up-regulation of immune cell-related genes including neutrophil markers. To examine this correlation in detail, we generate mice that lack Saa1-2 and investigate immune-cell phenotypes. RNA-seq experiments reveal that deletion of Saa1-2 does not strongly affect 4T1-induced activation of immune cell-related genes in the liver and bone marrow. Flow cytometry experiments demonstrate the dispensable roles of SAA1-2 in cancer-dependent neutrophil infiltration to the liver. This study clarifies the negligible contribution of SAA1-2 proteins in systemic inflammation in the 4T1 breast cancer model.Competing Interest StatementThe authors have declared no competing interest.