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Targeting cancer stem-like cells in glioblastoma and colorectal cancer through metabolic pathways

机译:通过代谢途径靶向胶质母细胞瘤和结肠直肠癌中的癌症干细胞

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摘要

Cancer stem-like cells (CSCs) are thought to be the main cause of tumor occurrence, progression and therapeutic resistance. Strong research efforts in the last decade have led to the development of several tailored approaches to target CSCs with some very promising clinical trials underway; however, until now no anti-CSC therapy has been approved for clinical use. Given the recent improvement in our understanding of how onco-proteins can manipulate cellular metabolic networks to promote tumorigenesis, cancer metabolism research may well lead to innovative strategies to identify novel regulators and downstream mediators of CSC maintenance. Interfering with distinct stages of CSC-associated metabolics may elucidate novel, more efficient strategies to target this highly malignant cell population. Here recent discoveries regarding the metabolic properties attributed to CSCs in glioblastoma (GBM) and malignant colorectal cancer (CRC) were summarized. The association between stem cell markers, the response to hypoxia and other environmental stresses including therapeutic insults as well as developmentally conserved signaling pathways with alterations in cellular bioenergetic networks were also discussed. The recent developments in metabolic imaging to identify CSCs were also summarized. This summary should comprehensively update basic and clinical scientists on the metabolic traits of CSCs in GBM and malignant CRC.
机译:癌症干细胞(CSCs)被认为是肿瘤发生,进展和治疗性的主要原因。过去十年的强劲研究努力导致开发几种定制的方法,以瞄准CSCS,在进行中有一些非常有前途的临床试验;然而,直到现在,没有抗CSC治疗已被批准用于临床使用。鉴于最近的改进我们对如何操纵蜂窝代谢网络以促进肿瘤发生,癌症代谢研究可能会导致识别新型监管机构和CSC维护下游介质的创新策略。干扰CSC相关代谢的不同阶段可以阐明新的,更有效的策略来靶向这种高度恶性细胞群体。这里总结了关于血母细胞瘤(GBM)和恶性结肠直肠癌(CRC)中归因于CSCs的代谢性质的发现。还讨论了干细胞标志物之间的关系,对缺氧和其他环境压力的反应,包括治疗性侮辱以及具有细胞生物生物能量网络的改变的发育挽救的信号通路。还总结了最近代谢成像的发展,以鉴定CSCs。本发明摘要应全面更新基本和临床科学家依赖于GBM和恶性CRC的CSC的代谢性状。

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