PT  - JOURNAL ARTICLE
AU  - Chenfeng He
AU  - Riyo Konishi
AU  - Ayano Harata
AU  - Yuki Nakamura
AU  - Rin Mizuno
AU  - Mayuko Yoda
AU  - Masakazu Toi
AU  - Kosuke Kawaguchi
AU  - Shinpei Kawaoka
TI  - Serum amyloid alpha 1-2 are not required for systemic inflammation in the 4T1 murine breast cancer model
AID  - 10.1101/2022.09.26.509617
DP  - 2022 Jan 01
TA  - bioRxiv
PG  - 2022.09.26.509617
4099  - http://biorxiv.org/content/early/2022/09/28/2022.09.26.509617.short
4100  - http://biorxiv.org/content/early/2022/09/28/2022.09.26.509617.full
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.