Neoadjuvant therapy alters the collagen architecture of pancreatic cancer tissue via Ephrin-A5.


Journal

British journal of cancer
ISSN: 1532-1827
Titre abrégé: Br J Cancer
Pays: England
ID NLM: 0370635

Informations de publication

Date de publication:
03 2022
Historique:
received: 28 09 2020
accepted: 10 11 2021
revised: 26 10 2021
pubmed: 27 11 2021
medline: 11 3 2022
entrez: 26 11 2021
Statut: ppublish

Résumé

The treatment of pancreatic cancer (PDAC) remains clinically challenging, and neoadjuvant therapy (NAT) offers down staging and improved surgical resectability. Abundant fibrous stroma is involved in malignant characteristic of PDAC. We aimed to investigate tissue remodelling, particularly the alteration of the collagen architecture of the PDAC microenvironment by NAT. We analysed the alteration of collagen and gene expression profiles in PDAC tissues after NAT. Additionally, we examined the biological role of Ephrin-A5 using primary cultured cancer-associated fibroblasts (CAFs). The expression of type I, III, IV, and V collagen was reduced in PDAC tissues after effective NAT. The bioinformatics approach provided comprehensive insights into NAT-induced matrix remodelling, which showed Ephrin-A signalling as a likely pathway and Ephrin-A5 (encoded by EFNA5) as a crucial ligand. Effective NAT reduced the number of Ephrin-A5 These results suggest that effective NAT changes the extracellular matrix with collagen profiles through CAFs and their Ephrin-A5 expression.

Sections du résumé

BACKGROUND
The treatment of pancreatic cancer (PDAC) remains clinically challenging, and neoadjuvant therapy (NAT) offers down staging and improved surgical resectability. Abundant fibrous stroma is involved in malignant characteristic of PDAC. We aimed to investigate tissue remodelling, particularly the alteration of the collagen architecture of the PDAC microenvironment by NAT.
METHODS
We analysed the alteration of collagen and gene expression profiles in PDAC tissues after NAT. Additionally, we examined the biological role of Ephrin-A5 using primary cultured cancer-associated fibroblasts (CAFs).
RESULTS
The expression of type I, III, IV, and V collagen was reduced in PDAC tissues after effective NAT. The bioinformatics approach provided comprehensive insights into NAT-induced matrix remodelling, which showed Ephrin-A signalling as a likely pathway and Ephrin-A5 (encoded by EFNA5) as a crucial ligand. Effective NAT reduced the number of Ephrin-A5
CONCLUSION
These results suggest that effective NAT changes the extracellular matrix with collagen profiles through CAFs and their Ephrin-A5 expression.

Identifiants

pubmed: 34824448
doi: 10.1038/s41416-021-01639-9
pii: 10.1038/s41416-021-01639-9
pmc: PMC8854423
doi:

Substances chimiques

Antineoplastic Agents 0
Ephrin-A5 0
Collagen 9007-34-5

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

628-639

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

Kosei Nakajima (K)

Division of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Department of Analytical Pathology, National Cancer Center Research Institute, Tokyo, Japan.

Yoshinori Ino (Y)

Division of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Department of Analytical Pathology, National Cancer Center Research Institute, Tokyo, Japan.

Chie Naito (C)

Division of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Department of Analytical Pathology, National Cancer Center Research Institute, Tokyo, Japan.

Satoshi Nara (S)

Hepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.

Mari Shimasaki (M)

Division of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Department of Analytical Pathology, National Cancer Center Research Institute, Tokyo, Japan.

Utako Ishimoto (U)

Division of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Department of Analytical Pathology, National Cancer Center Research Institute, Tokyo, Japan.

Toshimitsu Iwasaki (T)

Division of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Department of Analytical Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Hepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.

Noriteru Doi (N)

Division of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Department of Analytical Pathology, National Cancer Center Research Institute, Tokyo, Japan.

Minoru Esaki (M)

Hepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.

Yoji Kishi (Y)

Hepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.

Kazuaki Shimada (K)

Hepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.

Nobuyoshi Hiraoka (N)

Division of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan. nhiraoka@ncc.go.jp.
Department of Analytical Pathology, National Cancer Center Research Institute, Tokyo, Japan. nhiraoka@ncc.go.jp.

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