iiinova — where your digital self keeps evolving

We are based @ibbtec.bsky.social in Santander, Spain. We are part of #University of Cantabria and @csic.es. We are funded through @erc.europa.eu @contracancerinv.bsky.social and @ageinves.bsky.social. We will support the scientific+professional development of the researcher that fills the position.

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We have developed a model to investigate this process in detail and generated intriguing and exciting data that we aim to exploit in coming months. We have additional resources (clinical data, bioinformatics, molecular characterization) snd collaborations in place.

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This is an exciting project at the interphase of cancer biology and bioengineering, employing organ-on-chip approaches to describe how CAFs influence abnormal vascularization and drug perfusion in cancer.

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JOB ALERT!! 🧪 We are offering a postdoc position within our “antiCAFing” ERC-CoG project to investigate the interplay CAFs:endothelial cells and its impact in aberrant vascularization in tumors. More details below 👇. Please spread the word.

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Thanks to all the authors, funding agencies (@contracancerinv.bsky.social, @erc.europa.eu, #AEI), and institutions (@univcantabria.bsky.social, @csic.es) that support our work. 11/11 END!

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Additionally, our findings establish a mechanistic link between proteostasis and mechanotransduction via the HSP90α-YAP axis and its impact in cancer development, with potential relevance in other contexts where YAP activity is implicated. 10/11

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To our knowledge, this is the first study demonstrating the role of HSP90 in modulating #CAF behaviour and #TME characteristics, opening intriguing therapeutic avenues. 9/11

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Notably, this regulation is particularly relevant in mechanically stressed environments like CAFs, where mechanotransduction dominates over Hippo-dependent control. 8/11

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While previous studies linked HSP90 to heat-shock-induced YAP activation via the Hippo pathway (Luo, Nat Cell Biol 2020), our findings describe a distinct mechanism that operates under normal temperature conditions, emphasizing a direct interaction between HSP90α and YAP. 7/11

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This mechanism was validated in non-tumoral contexts employing emergent vasculogenesis models in microfluidic devices, underscoring the broader relevance of the HSP90α-YAP axis beyond CAFs. 6/11

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We identify the mechanotransducer YAP as a key effector of HSP90α. YAP is activated in CAFs through mechanotransduction, playing a critical role in CAF function. e show that HSP90α depletion compromises YAP stability, and that YAP is the main mediator of HSP90α functions in CAFs. 5/11

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Our findings reveal a crucial role for the master chaperone HSP90α in shaping CAF functionality, influencing extracellular matrix (ECM) remodelling, tumour growth, and dissemination in experimental breast cancer models. 4/11

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This is exciting because the pro-tumorigenic function of HSP90 and proteostasis mechanisms has not been considered outside the cell autonomous context of cancer cells. 3/11

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Through comprehensive gene expression analyses of human cancer stroma + unbiased chemical genomics approaches, we show that HSP90-dependent transcriptional programs are a consistent feature of CAFs associated with aggressive #TME and poor patient prognosis. 2/11

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Proteostasis control via HSP90α sustains YAP activity to drive aggressive behaviours in cancer-associated fibroblasts

New preprint alert 🚨 We are pleased to share our most recent story about how #CAFs rely on stress responses and proteostasis control to maintain their aberrantly activated state. A work spearheaded by Silvia Dominguez in my lab🧪. doi.org/10.1101/2025... 🧵1/11

doi.org

Cancers adapt proteostasis to cope with the burden of misfolded proteins, stabilize key signalling nodes and sustain their malignant behaviour. Tumour stroma is subjected to similar stresses, but how ...

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Thanks also to funding agencies and institutions (@contracancerinv.bsky.social, #AEi, @erc.europa.eu, #IBBTEC, @csic.es c.es, @univcantabria.bsky.social) for supporting our work, and to all cancer patients that inspire our research (6/6)

ivcantabria.bsky.social

Bluesky

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Bea’s project was a tough one, taking many different routes that didn’t pan out. Bea’s hard work, enthusiasm, ideas and technical ability make it work. So proud of how she carried out the project and defended it today. Cheers to her! (5/6)

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Interesting results linking stress and metabolic rearrangements in CAFs that we are currently preparing for publication. Stay tuned (4/6)

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Also, many thanks to the incredible group of people that form my team, for their input and assistance along the way and for the great working atmosphere. And to @fendtlab.bsky.social) for hosting Bea and helping us in this project (2/6)

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New PhD in the CalvoLab! Congratulations to Beatriz Rodriguez Coursier for her amazing work defending her PhD project. Thanks to the evaluating panel for the discussion and comments (Adan Pinto, Ana Villar, Esther Castellano)(1/6)

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Thanks also to funding agencies and institutions (#AECC, #AEi, #ERC, #IBBTEC, @csic.es, #unican) for supporting our work, and to all cancer patients that inspire our research.

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This work has projected our research to new directions and technologies, and it would have been impossible without the effort and input of Diane and Emad. So proud of how she carried out the project and defended it today. Cheers to her!!

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Emergent mechanical control of vascular morphogenesis

And that we could now address with the help of Emad through the development of microfluidic devices for emergent vascularization (see link for some clues). It took us a while to learn the techniques (thanks to our all collaborators!) but it was worth it. www.science.org/doi/10.1126/...

science.org

Stromal cells create a biomechanically suitable environment for endothelial cells to form microvascular networks.

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Also, many thanks to my sidewinder Javier Rodriguez for his inputs, assistance and co-direction, and to Emad Moeendarbary that helped us along the way. Also, a good time to reflect on the incredible group of people that form my team.

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