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Melanoma cells control the formation of a primary tumour niche by releasing microRNA-carrying melanosomes that are taken up by dermal fibroblasts leading to their activation.
Extracellular vesicles, such as exosomes, are important effectors in the formation of tumour-fostering niches. Pigmented melanosomes are now shown to have a relevant role in establishing a tumour niche in primary melanoma by reprogramming dermal fibroblasts into cancer-associated fibroblasts through the transfer of miR-211.
While the beneficial versus detrimental implications of the senescence-associated secretome remain an issue of debate, time-resolved analyses of its composition, regulatory mechanisms and functional consequences have been largely missing. The dynamic activity of NOTCH is now shown to direct two distinct senescence phenotypes, by first promoting a pro-senescent TGF-β1-dependent secretome, followed by a second wave of pro-inflammatory, senescence-clearing cytokines.
Weiss and colleagues report that the EMT transcription factors Snail and Slug control skeletal stem cell self-renewal and differentiation by forming transcriptional complexes with the co-activators YAP and TAZ.
Kim et al. demonstrate that sex hormones induce Mib1 expression in myofibres during puberty, initiating the conversion of cycling juvenile satellite cells into adult quiescent satellite cells.
At sites of cell adhesion to the matrix, integrins are coupled to the actin cytoskeleton through proteins such as talin. Sun et al. now identify Kank2 as an activator of talin that reduces force transmission across focal adhesions.
Zhou et al. show that GSK3β phosphorylates KDM1A and induces its deubiquitylation by USP22, leading to demethylation of histone H3K4 and glioblastoma progression.
Frede et al. use a chemical carcinogenesis model and lineage tracing to show that oesophageal tumour growth is driven by a single proliferating cancer cell population, suggesting the absence of a hierarchy of proliferating cells in this cancer type.
Hoare et al. find that NOTCH1 regulates the switch between two distinct senescence-associated secretomes—the TGF-β pathway and pro-inflammatory cytokines—and that its inhibition promotes clearance of oncogene-induced senescent liver cells.
Cha et al. report that the G9a/RelB axis represses Let-7b through DNMT3A, and sustains K-RAS and β-catenin signalling, thereby controlling the maintenance and function of colorectal-cancer-initiating cells.
Dror et al. report that melanoma-derived melanosomes carry miRNAs that induce primary fibroblast reprogramming into cancer-associated fibroblasts, and also induce the formation of a pro-tumorigenic niche.
It has been unclear how the relatively weak dynein motor can counterbalance kinesin forces during microtubule-dependent transport. Belyy et al. find that binding of dynactin and BICD2 increases the strength of the dynein motor.
