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Upregulation of C1-inhibitor in pancreatic cancer.
Oncotarget 2019; 10(55):5703-5712O

Abstract

Purpose

The complement system has recently sparked more interest in cancer research. The classical pathway is initiated by activation of the C1 complex, which irreversibly can be bound to and inhibited by C1-INH. We have previously shown that C1-INH is upregulated in human glioblastoma (astrocytoma grade IV) on both gene and protein level. We here examine whether the complement system seems to play a role also in pancreatic cancer.

Technique and results

We performed an expression analysis of complement associated genes in 36 pancreatic ductal adenocarcinoma tumors and matching normal pancreatic tissue samples from pancreatic cancer patients (data from the publicly available database GSE15471). C1-INH was significantly upregulated in the pancreatic cancer tissue. None of the downstream components of the cascade were significantly upregulated in the cancer samples as compared to the control samples, which is the same pattern as we found in glioblastoma. GO analysis showed that membrane attack complex came up as the second most significantly associated cellular component. Analyzing gene expression of C1-INH in the pancreatic cancer cell lines from primary tumors versus metastatic tumor revealed no difference for the two mRNA transcripts (GSE59357).

Interpretation

Analysis of gene expression of complement related genes shows an upregulation of C1-INH and a downregulation of downstream components. This could suggest that C1-INH plays a role also in pancreatic cancer.

Authors+Show Affiliations

The Rausing Laboratory, Division of Neurosurgery, Department of Clinical Sciences, Lund University, Lund, Sweden.The Rausing Laboratory, Division of Neurosurgery, Department of Clinical Sciences, Lund University, Lund, Sweden. Department of Clinical Chemistry, Skåne University Hospital, Scania, Sweden.The Rausing Laboratory, Division of Neurosurgery, Department of Clinical Sciences, Lund University, Lund, Sweden. Department of Neurosurgery, Skåne University Hospital, Scania, Sweden.The Rausing Laboratory, Division of Neurosurgery, Department of Clinical Sciences, Lund University, Lund, Sweden. Department of Neurosurgery, Skåne University Hospital, Scania, Sweden.The Rausing Laboratory, Division of Neurosurgery, Department of Clinical Sciences, Lund University, Lund, Sweden. Department of Neurosurgery, Skåne University Hospital, Scania, Sweden.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31620245

Citation

Osther, Kurt, et al. "Upregulation of C1-inhibitor in Pancreatic Cancer." Oncotarget, vol. 10, no. 55, 2019, pp. 5703-5712.
Osther K, Förnvik K, Liljedahl E, et al. Upregulation of C1-inhibitor in pancreatic cancer. Oncotarget. 2019;10(55):5703-5712.
Osther, K., Förnvik, K., Liljedahl, E., Salford, L. G., & Redebrandt, H. N. (2019). Upregulation of C1-inhibitor in pancreatic cancer. Oncotarget, 10(55), pp. 5703-5712. doi:10.18632/oncotarget.27191.
Osther K, et al. Upregulation of C1-inhibitor in Pancreatic Cancer. Oncotarget. 2019 Oct 1;10(55):5703-5712. PubMed PMID: 31620245.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Upregulation of C1-inhibitor in pancreatic cancer. AU - Osther,Kurt, AU - Förnvik,Karolina, AU - Liljedahl,Emma, AU - Salford,Leif G, AU - Redebrandt,Henrietta Nittby, Y1 - 2019/10/01/ PY - 2019/06/29/received PY - 2019/08/16/accepted PY - 2019/10/18/entrez PY - 2019/10/18/pubmed PY - 2019/10/18/medline KW - C1-inhibitor KW - cancer KW - complement system KW - immunotherapy KW - pancreatic cancer SP - 5703 EP - 5712 JF - Oncotarget JO - Oncotarget VL - 10 IS - 55 N2 - Purpose: The complement system has recently sparked more interest in cancer research. The classical pathway is initiated by activation of the C1 complex, which irreversibly can be bound to and inhibited by C1-INH. We have previously shown that C1-INH is upregulated in human glioblastoma (astrocytoma grade IV) on both gene and protein level. We here examine whether the complement system seems to play a role also in pancreatic cancer. Technique and results: We performed an expression analysis of complement associated genes in 36 pancreatic ductal adenocarcinoma tumors and matching normal pancreatic tissue samples from pancreatic cancer patients (data from the publicly available database GSE15471). C1-INH was significantly upregulated in the pancreatic cancer tissue. None of the downstream components of the cascade were significantly upregulated in the cancer samples as compared to the control samples, which is the same pattern as we found in glioblastoma. GO analysis showed that membrane attack complex came up as the second most significantly associated cellular component. Analyzing gene expression of C1-INH in the pancreatic cancer cell lines from primary tumors versus metastatic tumor revealed no difference for the two mRNA transcripts (GSE59357). Interpretation: Analysis of gene expression of complement related genes shows an upregulation of C1-INH and a downregulation of downstream components. This could suggest that C1-INH plays a role also in pancreatic cancer. SN - 1949-2553 UR - https://www.unboundmedicine.com/medline/citation/31620245/Upregulation_of_C1-inhibitor_in_pancreatic_cancer L2 - http://www.impactjournals.com/oncotarget/misc/linkedout.php?pii=27191 DB - PRIME DP - Unbound Medicine ER -