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Abstract At the early stage of tumor progression, fibroblasts are located at the outer edges of the tumor, forming an encasing layer around it. In this work, we have developed a 3D in vitro model where fibroblasts’ layout resembles the structure seen in carcinoma in situ. We use a microfluidic encapsulation technology to co-culture fibroblasts and cancer cells within hollow, permeable, and elastic alginate shells. We find that in the absence of spatial constraint, fibroblasts and cancer cells do not mix but segregate into distinct aggregates composed of individual cell types. However, upon confinement, fibroblasts enwrap cancer cell spheroid. Using a combination of biophysical methods and live imaging, we find that buildup of compressive stress is required to induce fibroblasts spreading over the aggregates of tumor cells. We propose that compressive stress generated by the tumor growth might be a mechanism that prompts fibroblasts to form a capsule around the tumor.

Ivashenka et al. report that galectin-3 (Gal3) binding to lactotransferrin drives its transcytosis in enterocytes. Such trafficking is Gal3- and glycosphingolipid-dependent, and Gal3 is found in clathrin-independent carriers. These findings suggest that polarized trafficking across the intestinal barrier relies on this glycolipid and lectin (GL-Lect)-mediated endocytosis.

Caveolae are plasma membrane invaginations playing crucial functions, like signal transduction and mechanoprotection. Here, the authors show that caveolae contribute to skin pigmentation by integrating the biochemical and mechanical response of epidermal melanocytes to extracellular cues.

Mechanical forces are sensed by cells and can alter plasma membrane properties, but biochemical changes underlying this are not clear. Here the authors show tension is sensed by c-Abl and FBP17, which couples changes in mechanical tension to remodelling of the plasma membrane and actin cytoskeleton.

Caveolae are mechanosensors and mutations of their coat proteins are implicated in muscle disorders, but molecular mechanisms are unclear. Here, the authors show that caveolae can regulate IL6/STAT3 signaling in muscle cells under stress, and that dystrophy related Cav3 mutant myotubes have reduced caveolae and upregulated IL6 signaling.

Endocytosis of the type I interferon receptor (IFNAR) is required for JAK/STAT signalling. Here the authors show that the internalized IFNAR1 and IFNAR2 subunits are differentially sorted by the retromer complex at the early endosome and this controls JAK/STAT signalling and gene transcription.