CCR – Lecture Series
Venue: Lecture Hall B2, Borschkegasse 4a
Time: Monday, March 2nd, 2026 at 13:00 PM
Host: Juliane Winkler
Programm
Tumor-ECM crosstalk in cancer progression
Johanna Ivaska
University of Turku
Tissue homeostasis relies on the spatial organization of distinct cell types and the
surrounding extracellular matrix (ECM), where integrin-mediated adhesion and actin
cytoskeleton dynamics regulate cellular identity, migration, and invasion. Our previous
work highlighted that normal stromal architecture can suppress breast cancer aggression
and even reprogram malignant cells towards a more benign state. Expanding this concept,
we investigated mechanobiological crosstalk in two distinct malignancies. In vocal fold
cancer (VFC), we identified increased ECM deposition and tissue stiffening correlating
with disease progression, receptor heterogeneity, and collective migration. Physiological
mechanical cues, such as stretching and vibration, attenuate nuclear β-catenin and YAP
signaling, suggesting that VFC is a mechanically sensitive tumor. YAP-TEAD inhibition
emerges as a potential therapeutic strategy. In mucinous colorectal carcinoma (MUC CRC),
we uncover a collagen–α2β1-integrin–SorLA axis regulating tumor polarity. This pathway
reinforces HER2/HER3 signaling and maintains apical-in polarity, with HER2-targeting
antibodies reversing polarity and impeding metastasis. Together, our findings highlight
diverse, tissue-specific mechanotransduction mechanisms that reshape tumor–stroma
interactions and offer novel avenues for therapeutic intervention.