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Cited by 28TGF-β signaling in diseasesInflammatory mediators and NSAID effectsSignaling Pathways in Disease

The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.

Regulation of Transforming Growth Factor-β-dependent Cyclooxygenase-2 Expression in Fibroblasts

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Matsumura, Takayoshi, Suzuki, Toru, Aizawa, Kenichi, Sawaki, Daigo, Munemasa, Yoshiko, Ishida, Junichi, Nagai, Ryozo·2009·Journal of Biological Chemistry
DOI 10.1074/jbc.m109.014639PMC PMC2791015
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Abstract

Abnormal transforming growth factor-β (TGF-β) signaling is a critical contributor to the pathogenesis of various human diseases ranging from tissue fibrosis to tumor formation. Excessive TGF-β signaling stimulates fibrotic responses. Recent research has focused in the main on the antiproliferative effects of TGF-β in fibroblasts, and it is presently understood that TGF-β-stimulated cyclooxygenase-2 (COX-2) induction in fibroblasts is essential for antifibroproliferative effects of TGF-β. Both TGF-β and COX-2 have been implicated in tumor growth, invasion, and metastasis, and therefore tumor-associated fibroblasts are a recent topic of interest. Here we report the identification of positive and negative regulatory factors of COX-2 expression induced by TGF-β as determined using proteomic approaches. We show that TGF-β coordinately up-regulates three factors, heterogeneous nuclear ribonucleoprotein A/B (HNRPAB), nucleotide diphosphate kinase A (NDPK A), and nucleotide diphosphate kinase A (NDPK B). Functional pathway analysis showed that HNRPAB augments mRNA and protein levels of COX-2 and subsequent prostaglandin E2 (PGE2) production by suppressing degradation of COX-2 mRNA. In contrast, NDPK A and NDPK B attenuated mRNA and protein levels of COX-2 by affecting TGF-β-Smad2/3/4 signaling at the receptor level. Collectively, we report on a new regulatory pathway of TGF-β in controlling expression of COX-2 in fibroblasts, which advances our understanding of pathophysiological mechanisms of TGF-β. Abnormal transforming growth factor-β (TGF-β) signaling is a critical contributor to the pathogenesis of various human diseases ranging from tissue fibrosis to tumor formation. Excessive TGF-β signaling stimulates fibrotic responses. Recent research has focused in the main on the antiproliferative effects of TGF-β in fibroblasts, and it is presently understood that TGF-β-stimulated cyclooxygenase-2 (COX-2) induction in fibroblasts is essential for antifibroproliferative effects of TGF-β. Both TGF-β and COX-2 have been implicated in tumor growth, invasion, and metastasis, and therefore tumor-associated fibroblasts are a recent topic of interest. Here we report the identification of positive and negative regulatory factors of COX-2 expression induced by TGF-β as determined using proteomic approaches. We show that TGF-β coordinately up-regulates three factors, heterogeneous nuclear ribonucleoprotein A/B (HNRPAB), nucleotide diphosphate kinase A (NDPK A), and nucleotide diphosphate kinase A (NDPK B). Functional pathway analysis showed that HNRPAB augments mRNA and protein levels of COX-2 and subsequent prostaglandin E2 (PGE2) production by suppressing degradation of COX-2 mRNA. In contrast, NDPK A and NDPK B attenuated mRNA and protein levels of COX-2 by affecting TGF-β-Smad2/3/4 signaling at the receptor level. Collectively, we report on a new regulatory pathway of TGF-β in controlling expression of COX-2 in fibroblasts, which advances our understanding of pathophysiological mechanisms of TGF-β.

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Crossref · 10.1074/jbc.m109.014639

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  • TGF-β influences CAF expression of cytokines and chemokines that act on cancer, endothelial and/or immune cells, such as HGF, VEGF, IL-6, IL-8, MCP1, PGE2 and CXCL12.

    “Finally, TGF-β influences CAF expression of cytokines and chemokines that act on cancer, endothelial and/or immune cells, such as HGF245, VEGF, IL-6, IL-8, MCP1, PGE2 and CXCL12229,257–262.”

    From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [262]

  • TGF-β's pro-angiogenic activities include expression of angiogenic factors, including VEGF-A.

    “and expression of angiogenic factors, including VEGF-A262,268.”

    From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [262]

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  1. Sonoshita, 2002, Cancer Res., 62, 6846

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Metadata

Authors
Matsumura, T., Suzuki, T., Aizawa, K., Sawaki, D., Munemasa, Y., Ishida, J., & Nagai, R.
Affiliations
The University of Tokyo (JP)
Corresponding author
  • Suzuki, Toru
  • Nagai, Ryozo
ORCID
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2009-12
Volume
284
Issue
51
Pages
35861-35871
ISSN
0021-9258 (ISSN-L)
DOI
10.1074/jbc.m109.014639
PMC
PMC2791015
OpenAlex
W2030516172
Cited by
28
References
47
Citations by year
2024: 1 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 1 · 2015: 3 · 2014: 6 · 2013: 1 · 2012: 1
FWCI
0.54
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
  • Health Sciences › Medicine › Pharmacology (medical) › Inflammatory mediators and NSAID effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
TGF-beta, cyclooxygenase-2, fibroblasts, mRNA stability, prostaglandin E2, cancer-associated fibroblasts, fibrosis, gene expression regulation, proteomic screen
MeSH terms
Animals, Cell Line, Fibroblasts, Humans, Repressor Proteins, RNA, Messenger, Dinoprostone, Signal Transduction, Up-Regulation, Gene Expression Regulation, Enzymologic, Heterogeneous-Nuclear Ribonucleoprotein Group A-B, Mice, Cyclooxygenase 2, Smad Proteins, Transforming Growth Factor beta1, NM23 Nucleoside Diphosphate Kinases

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