Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
The epithelial to mesenchymal transition (EMT) has been recently associated with a stem cell phenotype. In breast cancer cell lines and tumours, p53 directly targets the expression of microRNAs that have been shown to inhibit EMT and stem cells regulators.
Cancer cells preferentially use aerobic glycolysis to generate ATP, consuming glucose in the process. The tumour suppressor p53 is now shown to suppress glucose consumption by inhibiting the pentose phosphate pathway (PPP). Tumour-associated p53 mutations lack this inhibitory effect.
Aneploidy is frequently observed in cancer. It is now shown that aneploidy can arise by entosis, the process of live cell internalisation by a neighbouring cell. The internalised cell can interfere with host cell division and disrupt the formation of the contractile actin ring resulting in cytokinesis defects and aneuploidy.
p114RhoGEF promotes RhoA activation at epithelial junctions. The junctional adaptor cingulin recruits p114RhoGEF to junctions, where it regulates junction formation through RhoA, Rock II and myosin II.
The cellular mechanisms that modulate morphogen gradient interpretation in tissue have been debated. In vivo fluorescence correlation spectroscopy and automated image analysis show that modulation of endocytic trafficking affects FGF8 target-gene expression without an effect on the FGF8 gradient itself.
Mammalian nuclear bodies are involved in various aspects of nuclear function and contain RNAs. Tethering of specific RNA transcripts to a genomic location allows de novo assembly of the nuclear bodies that normally contain these transcripts.