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Endogenous human microRNAs that suppress breast cancer metastasis
It is shown that restoring the expression of these microRNAs in malignant cells suppresses lung and bone metastasis by human cancer cells in vivo, and miR-126 restoration reduces overall tumour growth and proliferation, whereasmiR-335 inhibits metastatic cell invasion.
Breast cancer cells produce tenascin C as a metastatic niche component to colonize the lungs
Findings link TNC to pathways that support the fitness of metastasis-initiating breast cancer cells and highlight the relevance of TNC as an extracellular matrix protein of stem cell niches of the metastatic niche.
Regulation of neuronal morphology and function by the tumor suppressors Tsc1 and Tsc2
In post-mitotic, hippocampal pyramidal neurons of mice and rats, loss of Tsc1 or Tsc2 triggered enlargement of somas and dendritic spines and altered the properties of glutamatergic synapses, and perturbations of neuronal structure and function are likely to contribute to the pathogenesis of the neurological symptoms of TSC.
N6-methyladenosine marks primary microRNAs for processing
These findings reveal that the m6A mark acts as a key post-transcriptional modification that promotes the initiation of miRNA biogenesis and that METTL3 is sufficient to enhance miRNA maturation in a global and non-cell-type-specific manner.
A microRNA regulon that mediates endothelial recruitment and metastasis by cancer cells
Endogenous miR-126, an miRNA silenced in a variety of common human cancers, non-cell-autonomously regulates endothelial cell recruitment to metastatic breast cancer cells, in vitro and in vivo, and is identified as a key regulator of cancer-mediated endothelial recruitment.
Diverse receptive fields in the lateral geniculate nucleus during thalamocortical development
A Hebbian model whereby imprecise retinogeniculate connections help refine geniculocortical connections, sharpening both thalamocorticals topography and perhaps orientation selectivity is presented.