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The metabolic cross‐talk between epithelial cancer cells and stromal fibroblasts in ovarian cancer progression: Autophagy plays a role
Medicinal Research Reviews ( IF 13.3 ) Pub Date : 2017-09-19 , DOI: 10.1002/med.21473
Chanitra Thuwajit 1 , Alessandra Ferraresi 2 , Rossella Titone 2 , Peti Thuwajit 1 , Ciro Isidoro 2, 3
Affiliation  

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.

中文翻译:

卵巢癌进展中上皮癌细胞与基质成纤维细胞之间的代谢串扰:自噬发挥作用

癌细胞和基质细胞,包括(与癌相关的)成纤维细胞,脂肪细胞和免疫细胞,构成了一个混合的细胞生态系统,动态地影响着每个成分的行为,创造了最终有利于恶性克隆出现的条件。卵巢癌细胞释放可募集并激活基质成纤维细胞和免疫细胞的细胞因子,从而使基质中的炎症状态长期存在,从而阻碍免疫反应并促进癌症的生存和传播。此外,间质脉管系统通过提供或限制氧气和养分的可用性来影响细胞的代谢。自噬是一种具有稳态和生存功能的溶酶体分解代谢过程,会影响癌细胞的行为,影响各种过程,例如在新陈代谢恶劣条件下的存活,侵袭性生长,免疫和化学抗性的发展,茎样性质的维持以及休眠。此外,自噬参与了迁移细胞因子的分泌和信号传导。癌症相关的成纤维细胞可通过促炎性细胞因子的分泌以及自噬来源的代谢产物和底物的释放来影响卵巢癌细胞中自噬的实际水平。中断癌细胞与癌症相关的成纤维细胞之间的代谢串扰可能是阻止进展并预防卵巢癌复发的有效治疗策略。自噬参与了迁移细胞因子的分泌和信号传导。癌症相关的成纤维细胞可通过促炎性细胞因子的分泌以及自噬来源的代谢产物和底物的释放来影响卵巢癌细胞中自噬的实际水平。中断癌细胞与癌症相关的成纤维细胞之间的代谢串扰可能是阻止进展并预防卵巢癌复发的有效治疗策略。自噬参与了迁移细胞因子的分泌和信号传导。癌症相关的成纤维细胞可通过促炎性细胞因子的分泌以及自噬来源的代谢产物和底物的释放来影响卵巢癌细胞中自噬的实际水平。中断癌细胞与癌症相关的成纤维细胞之间的代谢串扰可能是阻止进展并预防卵巢癌复发的有效治疗策略。
更新日期:2017-09-19
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