Umeå University's logo

umu.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Targeting Tumor-Stromal Interactions in Pancreatic Cancer: Impact of Collagens and Mechanical Traits
Umeå University, Faculty of Medicine, Wallenberg Centre for Molecular Medicine at Umeå University (WCMM). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
Umeå University, Faculty of Medicine, Wallenberg Centre for Molecular Medicine at Umeå University (WCMM). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
Umeå University, Faculty of Medicine, Wallenberg Centre for Molecular Medicine at Umeå University (WCMM). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.ORCID iD: 0000-0002-7151-1137
Umeå University, Faculty of Medicine, Wallenberg Centre for Molecular Medicine at Umeå University (WCMM). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.ORCID iD: 0000-0002-5847-2778
2021 (English)In: Frontiers in Cell and Developmental Biology, E-ISSN 2296-634X, Vol. 9, article id 787485Article, review/survey (Refereed) Published
Abstract [en]

Pancreatic ductal adenocarcinoma (PDAC) has one of the worst outcomes among cancers with a 5-years survival rate of below 10%. This is a result of late diagnosis and the lack of effective treatments. The tumor is characterized by a highly fibrotic stroma containing distinct cellular components, embedded within an extracellular matrix (ECM). This ECM-abundant tumor microenvironment (TME) in PDAC plays a pivotal role in tumor progression and resistance to treatment. Cancer-associated fibroblasts (CAFs), being a dominant cell type of the stroma, are in fact functionally heterogeneous populations of cells within the TME. Certain subtypes of CAFs are the main producer of the ECM components of the stroma, with the most abundant one being the collagen family of proteins. Collagens are large macromolecules that upon deposition into the ECM form supramolecular fibrillar structures which provide a mechanical framework to the TME. They not only bring structure to the tissue by being the main structural proteins but also contain binding domains that interact with surface receptors on the cancer cells. These interactions can induce various responses in the cancer cells and activate signaling pathways leading to epithelial-to-mesenchymal transition (EMT) and ultimately metastasis. In addition, collagens are one of the main contributors to building up mechanical forces in the tumor. These forces influence the signaling pathways that are involved in cell motility and tumor progression and affect tumor microstructure and tissue stiffness by exerting solid stress and interstitial fluid pressure on the cells. Taken together, the TME is subjected to various types of mechanical forces and interactions that affect tumor progression, metastasis, and drug response. In this review article, we aim to summarize and contextualize the recent knowledge of components of the PDAC stroma, especially the role of different collagens and mechanical traits on tumor progression. We furthermore discuss different experimental models available for studying tumor-stromal interactions and finally discuss potential therapeutic targets within the stroma.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2021. Vol. 9, article id 787485
Keywords [en]
collagen, extracellular matrix, mechanical traits, pancreatic cancer, PDAC—pancreatic ductal adenocarcinoma, stroma
National Category
Cell and Molecular Biology Cancer and Oncology
Research subject
Oncology
Identifiers
URN: urn:nbn:se:umu:diva-190614DOI: 10.3389/fcell.2021.787485PubMedID: 34901028Scopus ID: 2-s2.0-85120962866OAI: oai:DiVA.org:umu-190614DiVA, id: diva2:1621700
Funder
EU, Horizon 2020, 861196Swedish Research Council, 2017-01531Region Västerbotten, RV-930167Region Västerbotten, VLL-832001Cancerforskningsfonden i Norrland, LP 21-2298Marianne and Marcus Wallenberg Foundation, MMW 2020.0189Swedish Cancer Society, CAN 2017/332Swedish Cancer Society, CAN 2017/827Swedish Cancer Society, 20 1339 PjFAvailable from: 2021-12-20 Created: 2021-12-20 Last updated: 2022-05-13Bibliographically approved

Open Access in DiVA

fulltext(2518 kB)223 downloads
File information
File name FULLTEXT01.pdfFile size 2518 kBChecksum SHA-512
041d22acd362f5ab7e196919298a41b5eba6df17d0ea561e9d9270fd8597f8ae83f97074c53b625084d210a28f6e7c69834fa8433b04d4212b0b67e8f1291d1d
Type fulltextMimetype application/pdf

Other links

Publisher's full textPubMedScopus

Authority records

Maneshi, ParniyanMason, JamesDongre, MiteshÖhlund, Daniel

Search in DiVA

By author/editor
Maneshi, ParniyanMason, JamesDongre, MiteshÖhlund, Daniel
By organisation
Wallenberg Centre for Molecular Medicine at Umeå University (WCMM)Oncology
In the same journal
Frontiers in Cell and Developmental Biology
Cell and Molecular BiologyCancer and Oncology

Search outside of DiVA

GoogleGoogle Scholar
Total: 223 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 366 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf