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Upregulation of C1-inhibitor in pancreatic cancer

Osther, Kurt LU ; Förnvik, Karolina LU orcid ; Liljedahl, Emma LU ; Salford, Leif G LU and Nittby Redebrandt, Henrietta LU (2019) In Oncotarget 10(55). p.5703-5712
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... (More)

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.

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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Oncotarget
volume
10
issue
55
pages
10 pages
publisher
Impact Journals
external identifiers
  • pmid:31620245
  • scopus:85072916859
ISSN
1949-2553
DOI
10.18632/oncotarget.27191
language
English
LU publication?
yes
id
cd971dbb-6869-48d8-a6e0-92f6b1b01c06
date added to LUP
2020-07-09 00:23:23
date last changed
2024-06-26 19:39:47
@article{cd971dbb-6869-48d8-a6e0-92f6b1b01c06,
  abstract     = {{<p>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.</p><p>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).</p><p>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.</p>}},
  author       = {{Osther, Kurt and Förnvik, Karolina and Liljedahl, Emma and Salford, Leif G and Nittby Redebrandt, Henrietta}},
  issn         = {{1949-2553}},
  language     = {{eng}},
  month        = {{10}},
  number       = {{55}},
  pages        = {{5703--5712}},
  publisher    = {{Impact Journals}},
  series       = {{Oncotarget}},
  title        = {{Upregulation of C1-inhibitor in pancreatic cancer}},
  url          = {{http://dx.doi.org/10.18632/oncotarget.27191}},
  doi          = {{10.18632/oncotarget.27191}},
  volume       = {{10}},
  year         = {{2019}},
}