Academic Journal
B cells enhance IL-1 beta driven invasiveness in triple negative breast cancer
| Title: | B cells enhance IL-1 beta driven invasiveness in triple negative breast cancer |
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| Authors: | Nicole J. Toney, Lynn M. Opdenaker, Lisa Frerichs, Shirin R. Modarai, Aihui Ma, Holly Archinal, Grace O. Ajayi, Jennifer Sims-Mourtada |
| Source: | Scientific Reports, Vol 15, Iss 1, Pp 1-16 (2025) |
| Publisher Information: | Nature Portfolio, 2025. |
| Publication Year: | 2025 |
| Collection: | LCC:Medicine LCC:Science |
| Subject Terms: | Breast cancer, Triple negative breast cancer, Interleukin 1 beta, B cells, NFkappa B, Medicine, Science |
| More Details: | Abstract Triple-negative breast cancer (TNBC) is an aggressive subtype often characterized by high lymphocyte infiltration, including tumor-infiltrating B cells (TIBs). These cells are present even in early stages of TNBC and associated with microinvasion. This study shows that co-culturing TNBC cells with B cells increases Interleukin-1β (IL-1β) expression and secretion. We further show that B cell-induced IL-1β activates NFκB signaling, leading to higher expression of target genes and promoting IL-1β-dependent increases in matrix metalloproteinase (MMP) activity, invasion, and migration. Immunohistochemical analysis of IL-1β and TIBs in triple-negative ductal carcinoma in situ (DCIS, n = 90) and invasive TNBC (n = 171) revealed that in DCIS, TIBs correlated with IL-1β expression and microinvasion, with IL-1β also linked to recurrence. In invasive TNBC, IL-1β expression correlated with TIB density and stage, with high IL-1β levels associated with poorer survival outcomes. These findings suggest that early B cell presence in TNBC can induce IL-1β secretion, enhancing invasion and mobility through IL-1β-NFκB signaling. This highlights the potential of IL-1 inhibitors as preventive and therapeutic options for hormone receptor-negative DCIS and TNBC. |
| Document Type: | article |
| File Description: | electronic resource |
| Language: | English |
| ISSN: | 2045-2322 |
| Relation: | https://doaj.org/toc/2045-2322 |
| DOI: | 10.1038/s41598-025-86064-1 |
| Access URL: | https://doaj.org/article/4191edd484bb4da2be72333a6e8f1ba2 |
| Accession Number: | edsdoj.4191edd484bb4da2be72333a6e8f1ba2 |
| Database: | Directory of Open Access Journals |
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| ISSN: | 20452322 |
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| DOI: | 10.1038/s41598-025-86064-1 |
| Published in: | Scientific Reports |
| Language: | English |