Suppr超能文献

钒-Schiff 碱配合物诱导人结直肠癌细胞系 HCT-116 凋亡。

Induction of apoptosis in human colorectal cancer cell line, HCT-116 by a vanadium- Schiff base complex.

机构信息

Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700 026, India.

Department of Pharmacology, Institute of Post Graduate Medical Education and Research, 244, A.J.C. Bose Road, Kolkata 700020, India.

出版信息

Biomed Pharmacother. 2017 Aug;92:509-518. doi: 10.1016/j.biopha.2017.05.108. Epub 2017 May 30.

Abstract

Vanadium compounds are well known for their therapeutic interventions against several diseases. Various biochemical attributes of vanadium complexes inspired us to evaluate the cancer cell killing efficacy of the vanadium complex, viz., vanadyl N-(2-hydroxyacetophenone) glycinate [VO(NG)]. Previously we showed that VO(NG) is an effective anticancer agent in in vitro and in vivo cancer models and imposed miniscule side effects. Herein we report that VO(NG) is significantly cytotoxic to various cancer cell lines. Furthermore, this redox active vanadyl complex altered the redox homeostatsis of many human cancer cell lines significantly. VO(NG) actuates programmed cell death in human colorectal carcinoma cells(HCT-116) through mitochondrial outer membrane permeabilization but in caspase independent manner, possibly by altering cellular redox status and by inflicting DNA damage. Thus, the present work is an attempt to provide many evidences regarding the potent and selective chemotherapeutic efficacy of the novel VO(NG).

摘要

钒化合物以其对多种疾病的治疗干预而闻名。钒配合物的各种生化特性激发了我们评估钒配合物,即[VO(NG)],的杀伤癌细胞的功效。我们之前的研究表明,VO(NG)是一种有效的体外和体内癌症模型中的抗癌剂,且副作用极小。在此,我们报告称,VO(NG)对多种癌细胞系具有显著的细胞毒性。此外,这种氧化还原活性的钒配合物显著改变了许多人类癌细胞系的氧化还原稳态。VO(NG)通过线粒体外膜通透性诱导人结直肠癌细胞(HCT-116)发生程序性细胞死亡,但不依赖于半胱天冬酶,可能是通过改变细胞氧化还原状态和造成 DNA 损伤。因此,本工作试图提供许多关于新型 VO(NG)的有效和选择性化学治疗功效的证据。

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