Durotaxis is a driver and potential therapeutic target in lung fibrosis and metastatic pancreatic cancer Article Swipe
Taslim A. Al-Hilal
,
Maria-Anna Chrysovergi
,
Paula Grasberger
,
Fei Liu
,
Vera Auernheimer
,
Yan Zhou
,
Zebin Xiao
,
Mark Anthony Leon Duque
,
Alba Santos
,
Tamanna Islam
,
Matteo Ligorio
,
Delphine Sicard
,
Clemens K. Probst
,
Vladimir Vrbanac
,
Tejaswini Reddi
,
Ludovic G. Vincent
,
Cassandra Happe
,
Edward Chaum
,
Charles R. Yates
,
K. Daneshvar
,
Alan C. Mullen
,
David T. Ting
,
Eric S. White
,
Raghu Kalluri
,
Christina M. Woo
,
Ellen Puré
,
Wolfgang H. Goldmann
,
José L. Alonso
,
Andrew M. Tager
,
Adam J. Engler
,
Daniel J. Tschumperlin
,
David Lagares
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1038/s41556-025-01697-8
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1038/s41556-025-01697-8
Durotaxis, cell migration along stiffness gradients, is linked to embryonic development, tissue repair and disease. Despite solid in vitro evidence, its role in vivo remains largely speculative. Here we demonstrate that durotaxis actively drives disease progression in vivo in mouse models of lung fibrosis and metastatic pancreatic cancer. In lung fibrosis, durotaxis directs fibroblast recruitment to sites of injury, where they undergo mechano-activation into scar-forming myofibroblasts. In pancreatic cancer, stiffening of the tumour microenvironment induces durotaxis of cancer cells, promoting metastatic dissemination. Mechanistically, durotaxis is mediated by focal adhesion kinase (FAK)–paxillin interaction, a mechanosensory module that links stiffness cues to transcriptional programmes via YAP signalling. To probe this genetically, we generated a FAK-FAT L994E knock-in mouse, which disrupts FAK–paxillin binding, blocks durotaxis and attenuates disease severity. Pharmacological inhibition of FAK–paxillin interaction with the small molecule JP-153 mimics these effects. Our findings establish durotaxis as a disease mechanism in vivo and support anti-durotactic therapy as a potential strategy for treating fibrosis and cancer.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1038/s41556-025-01697-8
- OA Status
- hybrid
- Cited By
- 2
- References
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- Related Works
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All OpenAlex metadata
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Durotaxis is a driver and potential therapeutic target in lung fibrosis and metastatic pancreatic cancerWork title
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articleOpenAlex work type
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enPrimary language
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2025Year of publication
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2025-09-01Full publication date if available
- Authors
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Taslim A. Al-Hilal, Maria-Anna Chrysovergi, Paula Grasberger, Fei Liu, Vera Auernheimer, Yan Zhou, Zebin Xiao, Mark Anthony Leon Duque, Alba Santos, Tamanna Islam, Matteo Ligorio, Delphine Sicard, Clemens K. Probst, Vladimir Vrbanac, Tejaswini Reddi, Ludovic G. Vincent, Cassandra Happe, Edward Chaum, Charles R. Yates, K. Daneshvar, Alan C. Mullen, David T. Ting, Eric S. White, Raghu Kalluri, Christina M. Woo, Ellen Puré, Wolfgang H. Goldmann, José L. Alonso, Andrew M. Tager, Adam J. Engler, Daniel J. Tschumperlin, David LagaresList of authors in order
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https://doi.org/10.1038/s41556-025-01697-8Publisher landing page
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YesWhether a free full text is available
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hybridOpen access status per OpenAlex
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2Total citation count in OpenAlex
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2025: 2Per-year citation counts (last 5 years)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.FAK-FAT | 113 |
| abstract_inverted_index.cancer, | 69 |
| abstract_inverted_index.cancer. | 48, 162 |
| abstract_inverted_index.directs | 53 |
| abstract_inverted_index.disease | 35, 125, 146 |
| abstract_inverted_index.induces | 75 |
| abstract_inverted_index.injury, | 59 |
| abstract_inverted_index.largely | 26 |
| abstract_inverted_index.remains | 25 |
| abstract_inverted_index.support | 151 |
| abstract_inverted_index.therapy | 153 |
| abstract_inverted_index.undergo | 62 |
| abstract_inverted_index.Abstract | 0 |
| abstract_inverted_index.actively | 33 |
| abstract_inverted_index.adhesion | 89 |
| abstract_inverted_index.binding, | 120 |
| abstract_inverted_index.disease. | 15 |
| abstract_inverted_index.disrupts | 118 |
| abstract_inverted_index.effects. | 139 |
| abstract_inverted_index.fibrosis | 44, 160 |
| abstract_inverted_index.findings | 141 |
| abstract_inverted_index.knock-in | 115 |
| abstract_inverted_index.mediated | 86 |
| abstract_inverted_index.molecule | 135 |
| abstract_inverted_index.strategy | 157 |
| abstract_inverted_index.treating | 159 |
| abstract_inverted_index.durotaxis | 32, 52, 76, 84, 122, 143 |
| abstract_inverted_index.embryonic | 10 |
| abstract_inverted_index.establish | 142 |
| abstract_inverted_index.evidence, | 20 |
| abstract_inverted_index.fibrosis, | 51 |
| abstract_inverted_index.generated | 111 |
| abstract_inverted_index.mechanism | 147 |
| abstract_inverted_index.migration | 3 |
| abstract_inverted_index.potential | 156 |
| abstract_inverted_index.promoting | 80 |
| abstract_inverted_index.severity. | 126 |
| abstract_inverted_index.stiffness | 5, 98 |
| abstract_inverted_index.Durotaxis, | 1 |
| abstract_inverted_index.attenuates | 124 |
| abstract_inverted_index.fibroblast | 54 |
| abstract_inverted_index.gradients, | 6 |
| abstract_inverted_index.inhibition | 128 |
| abstract_inverted_index.metastatic | 46, 81 |
| abstract_inverted_index.pancreatic | 47, 68 |
| abstract_inverted_index.programmes | 102 |
| abstract_inverted_index.stiffening | 70 |
| abstract_inverted_index.demonstrate | 30 |
| abstract_inverted_index.interaction | 131 |
| abstract_inverted_index.progression | 36 |
| abstract_inverted_index.recruitment | 55 |
| abstract_inverted_index.signalling. | 105 |
| abstract_inverted_index.development, | 11 |
| abstract_inverted_index.genetically, | 109 |
| abstract_inverted_index.interaction, | 92 |
| abstract_inverted_index.scar-forming | 65 |
| abstract_inverted_index.speculative. | 27 |
| abstract_inverted_index.FAK–paxillin | 119, 130 |
| abstract_inverted_index.dissemination. | 82 |
| abstract_inverted_index.mechanosensory | 94 |
| abstract_inverted_index.Pharmacological | 127 |
| abstract_inverted_index.anti-durotactic | 152 |
| abstract_inverted_index.myofibroblasts. | 66 |
| abstract_inverted_index.transcriptional | 101 |
| abstract_inverted_index.(FAK)–paxillin | 91 |
| abstract_inverted_index.Mechanistically, | 83 |
| abstract_inverted_index.microenvironment | 74 |
| abstract_inverted_index.mechano-activation | 63 |
| cited_by_percentile_year.max | 97 |
| cited_by_percentile_year.min | 95 |
| countries_distinct_count | 2 |
| institutions_distinct_count | 32 |
| citation_normalized_percentile.value | 0.94709186 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |