This week’s articles describe engineered exosomes for treating pancreatic cancer, the role of the endoplasmic reticulum in cancer cell apoptosis, the priming of brown fat for cold-induced thermogenesis, synapse loss in a mouse model of lupus, and communication between cells of different lineages during liver development.
CANCER
Targeting pancreatic cancer with exosomes
Kamerkar et al. engineered exosomes carrying an interfering RNA that targets an oncogenic form of KRAS commonly found in pancreatic cancer.
Endoplasmic reticulum calcium flux in cancer
Bononi et al. found that the tumor suppressor BRCA1-associated protein 1 (BAP1) promotes the release of Ca2+ from the endoplasmic reticulum and subsequent apoptosis by stabilizing an IP3 receptor.
Kuchay et al. report that inhibiting ubiquitin-dependent degradation of an IP3 receptor sensitizes PTEN-deficient tumors to photoradiation therapy by restoring the apoptosis-promoting release of Ca2+ from the endoplasmic reticulum.
METABOLISM
Priming the thermogenesis machinery
Emmett et al. found that histone deacetylase 3 (HDAC3) primes brown fat to generate heat in response to cold temperature.
NEUROSCIENCE
How lupus causes synapse loss
Bialas et al. report that interferons promote the loss of synapses in the brain in a mouse model of lupus by stimulating microglia to become reactive (see also McGlasson and Hunt).
DEVELOPMENTAL BIOLOGY
Interlineage communication in liver development
Using three-dimensional organoids, Camp et al. demonstrate that vascular endothelial growth factor (VEGF) signaling mediates crosstalk between different cell lineages during liver bud development.