摘要
背景:原癌基因和抑癌基因的突变使癌细胞无限增殖。因为它们拥有几乎所有的细胞增殖和存活机制,如健康的C。英语学习者,很难专门针对癌细胞在体内。目前的治疗在大多数情况下也对健康细胞有害。因此,这将是非常谨慎的目标规范癌细胞的FIC字符。由于癌细胞贪婪地利用葡萄糖和谷氨酰胺的生存和增殖,通过上调相关酶及其特定的亚型具有重要作用作为治疗干预的一部分,近年来人们一直关注与能量相关的代谢途径。 目的:总结同工酶在乳腺癌中高表达,能量代谢和其他重要的信号通路在调控细胞增殖相声角色,侵袭乳腺癌的转移与转移。 方法:从谷歌学者和PubMed上最近发表的文献中收集信息。在现有的情况下,体内结果在体外工程中更为重要。 结果:与许多其他癌症一样,乳腺癌对糖酵解依赖性增强,而不是线粒体呼吸,这是健康细胞的主要能量来源。癌细胞改变细胞能量系统有助于减少活性氧的水平,同时产生足够多的大分子——蛋白质、脂类和核苷酸以促进细胞增殖。改变的系统使细胞生长、增殖、转移和产生耐药性。代谢酶的同功酶在乳腺癌中表达及表达的程度不同亚型的酶不同。 结论:明确了解乳腺癌不同分子亚型中能量代谢的变化,将有助于治疗各种类型的乳腺癌。治疗方案。抗肿瘤药物或RNAi或两者相结合的靶向肿瘤细胞的特异性同工酶代谢酶在这篇文章中提到可以提供一个伟大的BRE的治疗方式乳腺癌。
关键词: 乳腺癌、糖酵解、TCA循环、磷酸戊糖途径、谷氨酰胺、原癌基因。
图形摘要
Current Cancer Drug Targets
Title:Potential Therapeutic Targets in Energy Metabolism Pathways of Breast Cancer
Volume: 17 Issue: 8
关键词: 乳腺癌、糖酵解、TCA循环、磷酸戊糖途径、谷氨酰胺、原癌基因。
摘要: Background: Mutations in proto-oncogenes and tumor suppressor genes make cancer cells proliferate indefinitely. As they possess almost all mechanisms for cell proliferation and survival like healthy cells, it is difficult to specifically target cancer cells in the body. Current treatments in most of the cases are harmful to healthy cells as well. Thus, it would be of great prudence to target specific characters of cancer cells. Since cancer cells avidly use glucose and glutamine to survive and proliferate by upregulating the relevant enzymes and their specific isoforms having important regulatory roles, it has been of great interest recently to target the energy-related metabolic pathways as part of the therapeutic interventions.
Objective: This paper summarizes the isozymes overexpressed in breast cancer, their roles of energy metabolism and cross-talks with other important signaling pathways in regulating proliferation, invasion and metastasis in breast cancer.
Method: Information has been collected from recently published literature available on Google Scholar and PubMed. Where available, in vivo results were given more importance over in vitro works.
Result: Like many other cancers, breast cancer shows increased dependence on glycolysis rather than mitochondrial respiration, the main energy source in healthy cells. Cancer cells alter the cellular energy system in a way that helps minimize level of reactive oxygen species and simultaneously produce enough macromolecules- proteins, lipids and nucleotides for cellular proliferation. The altered system enables the cells to grow, proliferate, metastasize and to develop drug resistance. Certain isozymes of metabolic enzymes are overexpressed in breast cancer and the degree of expression of these enzymes vary among subtypes.
Conclusion: A clear understanding of the variations of energy metabolism in different molecular subtypes of breast cancer would help in treating each type with a very customized, safer and efficient treatment regimen. Anti-cancer drugs or RNAi or combination of both targeting cancer cell specific isozymes of metabolic enzymes mentioned in this article could offer a great treatment modality for breast cancer.
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Cite this article as:
Potential Therapeutic Targets in Energy Metabolism Pathways of Breast Cancer, Current Cancer Drug Targets 2017; 17 (8) . https://dx.doi.org/10.2174/1568009617666170330150458
DOI https://dx.doi.org/10.2174/1568009617666170330150458 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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