LncRNA mediated metabolic reprogramming: the chief culprits of solid tumor malignant progression: an update review.

IF 3.9 2区 医学 Q2 NUTRITION & DIETETICS
Kun Fang, Huizhe Xu, Shuai Yuan, Xiaoxi Li, Xiaoyu Chen, Xiushi Fan, Xiaoxin Gao, Lu Zhang, Shulan Sun, Xudong Zhu
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引用次数: 0

Abstract

Metabolism reprogramming (MR) is one of the top ten hallmarks of malignant tumors. The aberrant activation of MR has been recognized as a critical contributory factor to the malignant progression of solid tumors. Moreover, various long non-coding RNAs (lncRNAs) are implicated in the aberrant activation of MR in solid tumor cells. Therefore, in this review, we mainly focus on summarizing the functional relevance and molecular mechanistic underpinnings of lncRNAs in modulating MR of solid tumors by targeting glucose metabolism, lipid metabolism, affecting mitochondrial function, and regulating interactions between tumor and non-tumor cells in tumor microenvironment. Besides, we also underscore the potential for constructing lncRNAs-centered tumor metabolic regulation networks and developing novel anti-tumor strategies by targeting lncRNAs and abnormal MR. Ultimately, this review seeks to offer new targets and avenues for the clinical treatment of solid tumors in the future.

LncRNA 介导的代谢重编程:实体瘤恶性进展的罪魁祸首:最新综述。
代谢重编程(MR)是恶性肿瘤的十大特征之一。MR的异常激活已被认为是实体瘤恶性进展的关键因素。此外,各种长非编码 RNA(lncRNA)也与实体瘤细胞中 MR 的异常激活有关。因此,在这篇综述中,我们主要总结了 lncRNAs 通过靶向葡萄糖代谢、脂质代谢、影响线粒体功能以及调节肿瘤微环境中肿瘤细胞和非肿瘤细胞之间的相互作用来调节实体瘤 MR 的功能相关性和分子机理基础。此外,我们还强调了构建以 lncRNAs 为中心的肿瘤代谢调控网络以及通过靶向 lncRNAs 和异常 MR 开发新型抗肿瘤策略的潜力。最终,这篇综述力图为未来实体瘤的临床治疗提供新的靶点和途径。
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来源期刊
Nutrition & Metabolism
Nutrition & Metabolism 医学-营养学
CiteScore
8.40
自引率
0.00%
发文量
78
审稿时长
4-8 weeks
期刊介绍: Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.
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