Mitochondrial signaling pathways and their role in cancer drug resistance

IF 4.4 2区 生物学 Q2 CELL BIOLOGY Cellular signalling Pub Date : 2024-08-05 DOI:10.1016/j.cellsig.2024.111329
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Abstract

Mitochondria, traditionally known as cellular powerhouses, now emerge as critical signaling centers influencing cancer progression and drug resistance. The review highlights the role that apoptotic signaling, DNA mutations, mitochondrial dynamics and metabolism play in the development of resistance mechanisms and the advancement of cancer. Targeted approaches are discussed, with an emphasis on managing mitophagy, fusion, and fission of the mitochondria to make resistant cancer cells more susceptible to traditional treatments. Additionally, metabolic reprogramming can be used to effectively target metabolic enzymes such GLUT1, HKII, PDK, and PKM2 in order to avoid resistance mechanisms. Although there are potential possibilities for therapy, the complex structure of mitochondria and their subtle role in tumor development hamper clinical translation. Novel targeted medicines are put forth, providing fresh insights on combating drug resistance in cancer. The study also emphasizes the significance of glutamine metabolism, mitochondrial respiratory complexes, and apoptotic pathways as potential targets to improve treatment effectiveness against drug-resistant cancers. Combining complementary and nanoparticle-based techniques to target mitochondria has demonstrated encouraging results in the treatment of cancer, opening doors to reduce resistance and enable individualized treatment plans catered to the unique characteristics of each patient. Suggesting innovative approaches such as drug repositioning and mitochondrial drug delivery to enhance the efficacy of mitochondria-targeting therapies, presenting a pathway for advancements in cancer treatment. This thorough investigation is a major step forward in the treatment of cancer and has the potential to influence clinical practice and enhance patient outcomes.

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线粒体信号通路及其在癌症耐药性中的作用。
线粒体历来被称为细胞的 "动力室",如今已成为影响癌症进展和耐药性的关键信号中心。这篇综述强调了凋亡信号、DNA 突变、线粒体动力学和新陈代谢在抗药性机制的发展和癌症进展中所起的作用。文章讨论了有针对性的方法,重点是管理线粒体的有丝分裂、融合和分裂,使抗药性癌细胞更容易接受传统疗法。此外,代谢重编程可用于有效靶向 GLUT1、HKII、PDK 和 PKM2 等代谢酶,以避免抗药性机制。虽然存在潜在的治疗可能性,但线粒体的复杂结构及其在肿瘤发展中的微妙作用阻碍了临床转化。研究提出了新的靶向药物,为对抗癌症耐药性提供了新的见解。研究还强调了谷氨酰胺代谢、线粒体呼吸复合物和细胞凋亡途径作为潜在靶点的重要性,以提高抗药性癌症的治疗效果。结合互补技术和基于纳米粒子的技术来靶向线粒体,在治疗癌症方面取得了令人鼓舞的成果,为减少耐药性和实现符合每位患者独特特征的个体化治疗方案打开了大门。提出了药物重新定位和线粒体给药等创新方法,以提高线粒体靶向疗法的疗效,为癌症治疗的进步提供了一条途径。这项深入研究是癌症治疗领域迈出的重要一步,有可能影响临床实践,改善患者预后。
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来源期刊
Cellular signalling
Cellular signalling 生物-细胞生物学
CiteScore
8.40
自引率
0.00%
发文量
250
审稿时长
27 days
期刊介绍: Cellular Signalling publishes original research describing fundamental and clinical findings on the mechanisms, actions and structural components of cellular signalling systems in vitro and in vivo. Cellular Signalling aims at full length research papers defining signalling systems ranging from microorganisms to cells, tissues and higher organisms.
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