Publication: The metabolic cross-talk between epithelial cancer cells and stromal fibroblasts in ovarian cancer progression: Autophagy plays a role
Issued Date
2018-07-01
Resource Type
ISSN
10981128
01986325
01986325
Other identifier(s)
2-s2.0-85039428869
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Mahidol University
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SCOPUS
Bibliographic Citation
Medicinal Research Reviews. Vol.38, No.4 (2018), 1235-1254
Suggested Citation
Chanitra Thuwajit, Alessandra Ferraresi, Rossella Titone, Peti Thuwajit, Ciro Isidoro The metabolic cross-talk between epithelial cancer cells and stromal fibroblasts in ovarian cancer progression: Autophagy plays a role. Medicinal Research Reviews. Vol.38, No.4 (2018), 1235-1254. doi:10.1002/med.21473 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/45117
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Title
The metabolic cross-talk between epithelial cancer cells and stromal fibroblasts in ovarian cancer progression: Autophagy plays a role
Abstract
© 2017 The Authors Medicinal Research Reviews Published by Wiley Periodicals, Inc. Cancer and stromal cells, which include (cancer-associated) fibroblasts, adipocytes, and immune cells, constitute a mixed cellular ecosystem that dynamically influences the behavior of each component, creating conditions that ultimately favor the emergence of malignant clones. Ovarian cancer cells release cytokines that recruit and activate stromal fibroblasts and immune cells, so perpetuating a state of inflammation in the stroma that hampers the immune response and facilitates cancer survival and propagation. Further, the stroma vasculature impacts the metabolism of the cells by providing or limiting the availability of oxygen and nutrients. Autophagy, a lysosomal catabolic process with homeostatic and prosurvival functions, influences the behavior of cancer cells, affecting a variety of processes such as the survival in metabolic harsh conditions, the invasive growth, the development of immune and chemo resistance, the maintenance of stem-like properties, and dormancy. Further, autophagy is involved in the secretion and the signaling of promigratory cytokines. Cancer-associated fibroblasts can influence the actual level of autophagy in ovarian cancer cells through the secretion of pro-inflammatory cytokines and the release of autophagy-derived metabolites and substrates. Interrupting the metabolic cross-talk between cancer cells and cancer-associated fibroblasts could be an effective therapeutic strategy to arrest the progression and prevent the relapse of ovarian cancer.