AI Article Synopsis
- - Malignant insulinoma is a rare and aggressive pancreatic tumor, but the mechanisms behind its development and spread are still not fully understood.
- - This study investigates the role of Serum amyloid P component (SAP) in insulinoma by using genetically modified mice, finding that the absence of SAP enhances tumor growth and metastasis.
- - The research indicates that SAP influences the secretion of a particular signaling molecule (CXCL12) from surrounding cancer-supporting cells, suggesting that targeting SAP could be a potential treatment for malignant insulinoma.
Article Abstract
Malignant insulinoma is an extremely rare type of functioning pancreatic neuroendocrine tumour with a high degree of malignancy and a high incidence of metastasis. However, it is still unclear how malignant insulinomas develop and metastasize. Serum amyloid P component (SAP), a member of the pentraxin protein family, is an acute-phase protein secreted by liver cells. The role of SAP in insulinoma and the related mechanism are still unknown. To determine the effect of SAP on insulinoma, we crossed Rip1-Tag2 mice, which spontaneously develop insulinoma, and SAP knockout (KO) mice to generate Rip1-Tag2;SAP mice. We found that SAP deletion significantly promoted the growth, invasion and metastasis of malignant insulinoma through C-X-C motif chemokine ligand 12 (CXCL12) secreted by cancer-associated fibroblasts (CAFs). Further study showed that SAP deletion promoted CXCL12 secretion by CAFs through the CXCR4/p38/ERK signalling pathway. These findings reveal a novel role and mechanism of SAP in malignant insulinoma and provide direct evidence that SAP may be a therapeutic agent for this disease.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11103456 | PMC |
| http://dx.doi.org/10.1111/jcmm.18397 | DOI Listing |
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