SAP deletion promotes malignant insulinoma progression by inducing CXCL12 secretion from CAFs via the CXCR4/p38/ERK signalling pathway
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 pentrax...
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| Published in: | Journal of cellular and molecular medicine Vol. 28; no. 10; pp. e18397 - n/a |
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| 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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| AbstractList | 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.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. 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. 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. 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. |
| Author | Mai, Xiaobin Qi, Cuiling Wang, Le Tang, Pei Wang, Lijing Wang, Yan Zheng, Lingyun Li, Jiangchao Zhang, Qianqian Zhan, Yaping Tu, Juan Jiang, Guangchun Xu, Shuo |
| AuthorAffiliation | 1 School of Basic Medical Sciences Guangdong Pharmaceutical University Guangzhou Guangdong China |
| AuthorAffiliation_xml | – name: 1 School of Basic Medical Sciences Guangdong Pharmaceutical University Guangzhou Guangdong China |
| Author_xml | – sequence: 1 givenname: Guangchun surname: Jiang fullname: Jiang, Guangchun organization: Guangdong Pharmaceutical University – sequence: 2 givenname: Shuo surname: Xu fullname: Xu, Shuo organization: Guangdong Pharmaceutical University – sequence: 3 givenname: Xiaobin surname: Mai fullname: Mai, Xiaobin organization: Guangdong Pharmaceutical University – sequence: 4 givenname: Juan surname: Tu fullname: Tu, Juan organization: Guangdong Pharmaceutical University – sequence: 5 givenname: Le surname: Wang fullname: Wang, Le organization: Guangdong Pharmaceutical University – sequence: 6 givenname: Lijing surname: Wang fullname: Wang, Lijing organization: Guangdong Pharmaceutical University – sequence: 7 givenname: Yaping surname: Zhan fullname: Zhan, Yaping organization: Guangdong Pharmaceutical University – sequence: 8 givenname: Yan surname: Wang fullname: Wang, Yan organization: Guangdong Pharmaceutical University – sequence: 9 givenname: Qianqian orcidid: 0000-0001-6481-0780 surname: Zhang fullname: Zhang, Qianqian organization: Guangdong Pharmaceutical University – sequence: 10 givenname: Lingyun surname: Zheng fullname: Zheng, Lingyun organization: Guangdong Pharmaceutical University – sequence: 11 givenname: Jiangchao surname: Li fullname: Li, Jiangchao organization: Guangdong Pharmaceutical University – sequence: 12 givenname: Pei surname: Tang fullname: Tang, Pei email: 657706120@qq.com organization: Guangdong Pharmaceutical University – sequence: 13 givenname: Cuiling orcidid: 0000-0002-4223-7562 surname: Qi fullname: Qi, Cuiling email: qicuiling12345@163.com organization: Guangdong Pharmaceutical University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38766687$$D View this record in MEDLINE/PubMed |
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| Keywords | CAF malignant insulinoma CXCL12 SAP insulinoma growth insulinoma metastasis |
| Language | English |
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| Snippet | Malignant insulinoma is an extremely rare type of functioning pancreatic neuroendocrine tumour with a high degree of malignancy and a high incidence of... |
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| SubjectTerms | Acute phase proteins Amyloid Amyloid P component Animals Antibodies Breast cancer CAF Cancer therapies Cancer-Associated Fibroblasts - metabolism Cancer-Associated Fibroblasts - pathology Cell culture Cell Line, Tumor Cell Proliferation Chemokine CXCL12 - genetics Chemokine CXCL12 - metabolism Chemokines CXCL12 CXCL12 protein CXCR4 protein Disease Progression Fibroblasts Gene Deletion Hepatocytes Humans Insulinoma Insulinoma - genetics Insulinoma - pathology insulinoma growth insulinoma metastasis Kinases Ligands Malignancy malignant insulinoma MAP Kinase Signaling System Medical research Metastases Metastasis Mice Mice, Knockout Neuroendocrine tumors Original p38 Mitogen-Activated Protein Kinases - metabolism Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Pentraxins Proteins Pulmonary fibrosis Receptors, CXCR4 - genetics Receptors, CXCR4 - metabolism SAP SAP protein Signal transduction Tumors |
| Title | SAP deletion promotes malignant insulinoma progression by inducing CXCL12 secretion from CAFs via the CXCR4/p38/ERK signalling pathway |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcmm.18397 https://www.ncbi.nlm.nih.gov/pubmed/38766687 https://www.proquest.com/docview/3061638740 https://www.proquest.com/docview/3057074683 https://pubmed.ncbi.nlm.nih.gov/PMC11103456 |
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