bims-stacyt Biomed News
on Paracrine crosstalk between cancer and the organism
Issue of 2019‒04‒21
two papers selected by
Cristina Muñoz Pinedo
L’Institut d’Investigació Biomèdica de Bellvitge
  1. Stress responses in stromal cells and tumor homeostasis.
  2. Adiponectin inhibits high glucose-induced angiogenesis via inhibiting autophagy in RF/6A cells.
  1. Pharmacol Ther. 2019 Apr 15. pii: S0163-7258(19)30061-0. [Epub ahead of print]
    Stress responses in stromal cells and tumor homeostasis.
    Ilio Vitale, Gwenola Manic, Claudia Galassi, Lorenzo Galluzzi.
      In most (if not all) solid tumors, malignant cells are outnumbered by their non-malignant counterparts, including immune, endothelial and stromal cells. However, while the mechanisms whereby cancer cells adapt to microenvironmental perturbations have been studied in great detail, relatively little is known on stress responses in non-malignant compartments of the tumor microenvironment. Here, we discuss the mechanisms whereby cancer-associated fibroblasts and other cellular components of the tumor stroma react to stress in the context of an intimate crosstalk with malignant, endothelial and immune cells, and how such crosstalk influences disease progression and response to treatment.
    Keywords:  autophagy; hypoxia; immunosuppressive metabolites; immunotherapy; mesenchymal stem cells; oxidative phosphorylation
    DOI:  https://doi.org/10.1016/j.pharmthera.2019.04.004
  2. J Cell Physiol. 2019 Apr 14.
    Adiponectin inhibits high glucose-induced angiogenesis via inhibiting autophagy in RF/6A cells.
    Rong Li, Junhui Du, Yang Yao, Guomin Yao, Xiaodi Wang.
      Adiponectin, one of the adipose-derived hormone with metabolic activity, has been reported to conversely affect angiogenesis of endothelial cells in vitro. The previous study in animal models has demonstrated that adiponectin has a protective role in retinal vascular injury following pathological stimuli. However, clinical research regarding the relationship between plasma adiponectin level and diabetic retinopathy (DR) are inconclusive. The aim of this study was to investigate the effect of adiponectin on high glucose-induced retinal angiogenesis and its association with autophagy by using rhesus choroid-retinal endothelial (RF-6A) cells as a model. We found that cell vitality decreased and cell migration and tube formation increased in the high-glucose group. Treatment with adiponectin or 3-methyladenine (3-MA, an autophagy inhibitor) increased cell viability and inhibited cell migration and tube formation. In the high-glucose group, the protein expression of Bax and apoptosis rate of cells increased and the expression of Bcl-2 decreased, whereas treatment with adiponectin or 3-MA reversed these results. Autophagy was activated in the high-glucose group to present as more LC3B fluorescent dots and higher expressions of LC3B, Atg5 proteins as well as lower expression of p62. Treatment with adiponectin or 3-MA inhibited autophagy by promoting the expression of p-PI3K, p-AKT, and p-mTOR when compared with the high-glucose group. The results of this study suggested that adiponectin inhibits high glucose-induced angiogenesis of RF/6A cells by inhibiting autophagy, and promotion of the PI3K/AKT/mTOR pathway might be involved in the anti-autophagy activities of adiponectin.
    Keywords:  adiponectin; angiogenesis; apoptosis; autophagy; diabetic retinopathy
    DOI:  https://doi.org/10.1002/jcp.28659
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