Filipe, Elysse C. and Velayuthar, Sipiththa and Philp, Ashleigh and Nobis, Max and Latham, Sharissa L. and Parker, Amelia L. and Murphy, Kendelle J. and Wyllie, Kaitlin and Major, Gretel S. and Contreras, Osvaldo and Mok, Ellie T. Y. and Enriquez, Ronaldo F. and McGowan, Suzanne and Feher, Kristen and Quek, Lake‐Ee and Hancock, Sarah E. and Yam, Michelle and Tran, Emmi and Setargew, Yordanos F. I. and Skhinas, Joanna N. and Chitty, Jessica L. and Phimmachanh, Monica and Han, Jeremy Z. R. and Cadell, Antonia L. and Papanicolaou, Michael and Mahmodi, Hadi and Kiedik, Beata and Junankar, Simon and Ross, Samuel E. and Lam, Natasha and Coulson, Rhiannon and Yang, Jessica and Zaratzian, Anaiis and Da Silva, Andrew M. and Tayao, Michael and Chin, Ian L. and Cazet, Aurélie and Kansara, Maya and Segara, Davendra and Parker, Andrew and Hoy, Andrew J. and Harvey, Richard P. and Bogdanovic, Ozren and Timpson, Paul and Croucher, David R. and Lim, Elgene and Swarbrick, Alexander and Holst, Jeff and Turner, Nigel and Choi, Yu Suk and Kabakova, Irina V. and Philp, Andrew and Cox, Thomas R. (2024) Tumor Biomechanics Alters Metastatic Dissemination of Triple Negative Breast Cancer via Rewiring Fatty Acid Metabolism. Advanced Science, 11 (23). ISSN 2198-3844
Full text not available from this repository.Abstract
In recent decades, the role of tumor biomechanics on cancer cell behavior at the primary site has been increasingly appreciated. However, the effect of primary tumor biomechanics on the latter stages of the metastatic cascade, such as metastatic seeding of secondary sites and outgrowth remains underappreciated. This work sought to address this in the context of triple negative breast cancer (TNBC), a cancer type known to aggressively disseminate at all stages of disease progression. Using mechanically tuneable model systems, mimicking the range of stiffness's typically found within breast tumors, it is found that, contrary to expectations, cancer cells exposed to softer microenvironments are more able to colonize secondary tissues. It is shown that heightened cell survival is driven by enhanced metabolism of fatty acids within TNBC cells exposed to softer microenvironments. It is demonstrated that uncoupling cellular mechanosensing through integrin beta1 blocking antibody effectively causes stiff primed TNBC cells to behave like their soft counterparts, both in vitro and in vivo. This work is the first to show that softer tumor microenvironments may be contributing to changes in disease outcome by imprinting on TNBC cells a greater metabolic flexibility and conferring discrete cell survival advantages.
| Item Type: | Article |
|---|---|
| Subjects: | R Medicine > R Medicine (General) |
| Depositing User: | Repository Administrator |
| Date Deposited: | 19 Dec 2024 00:33 |
| Last Modified: | 19 Dec 2024 00:33 |
| URI: | https://eprints.victorchang.edu.au/id/eprint/1553 |
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