Suppr超能文献

针对 Bcl-2 家族、TGF-β、Wnt/β-连环蛋白、RASSF 和 miRNA 调控信号通路的靶向治疗,探索治疗耐药肿瘤的新策略。

Emerging strategies for sensitization of therapy resistant tumors toward cancer therapeutics by targeting the Bcl-2 family, TGF-β, Wnt/β-Catenin, RASSF and miRNA regulated signaling pathways.

机构信息

Department of Biological Sciences, Sunway University, No. 5 Jalan Universiti, Bandar Sunway, 47500, Subang Jaya, Selangor, Malaysia.

Department of Biological Sciences, Sunway University, No. 5 Jalan Universiti, Bandar Sunway, 47500, Subang Jaya, Selangor, Malaysia.

出版信息

Int J Biochem Cell Biol. 2021 Aug;137:106016. doi: 10.1016/j.biocel.2021.106016. Epub 2021 Jun 1.

Abstract

Conventional chemotherapy relies on the cytotoxicity of chemo-drugs to inflict destructive effects on tumor cells. However, as most tumor cells develop resistance to chemo-drugs, small doses of chemo-drugs are unlikely to provide significant clinical benefits in cancer treatment while high doses of chemo-drugs have been shown to impact normal human cells negatively due to the non-specific nature and cytotoxicity associated with chemo-drugs. To overcome this challenge, sensitizations of tumor cells with bioactive molecules that specifically target the pro-survival and pro-apoptosis signaling pathways of the tumor cells are likely to increase the therapeutic impacts and improve the clinical outcomes by reducing the dependency and adverse effects associated with using high doses of chemo-drugs in cancer treatment. This review focuses on emerging strategies to enhance the sensitization of tumor cells toward cancer therapies based on our understanding of tumor cell biology and underlying signaling pathways.

摘要

传统的化疗依赖于化疗药物的细胞毒性对肿瘤细胞造成破坏性影响。然而,由于大多数肿瘤细胞对化疗药物产生耐药性,小剂量的化疗药物不太可能在癌症治疗中提供显著的临床益处,而高剂量的化疗药物由于与化疗药物相关的非特异性和细胞毒性,已被证明会对正常人类细胞产生负面影响。为了克服这一挑战,用生物活性分子对肿瘤细胞进行敏化,这些分子专门针对肿瘤细胞的生存和凋亡信号通路,可能会通过减少对癌症治疗中使用高剂量化疗药物的依赖性和不良反应,增加治疗效果并改善临床结果。本综述侧重于根据我们对肿瘤细胞生物学和潜在信号通路的理解,探讨增强肿瘤细胞对癌症治疗敏感性的新策略。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验