Weissenrieder Jillian S, Kevin Foskett J
Department of Physiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
Department of Cell and Developmental Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
J Cell Physiol. 2025 Sep;240(9):e70093. doi: 10.1002/jcp.70093.
Cancer is a leading cause of death in developed countries, despite many breakthroughs in targeted small molecule and immunotherapeutic interventions. A deeper understanding of the characteristics and processes that underlie malignancy will enable us to develop more effective therapeutic options to improve patient outcomes. One particular area of interest is in cancer cell metabolism. Even as early as the 1920s, Otto Warburg recognized dysregulated metabolism in cancerous cells. Altered metabolism may provide targetable nutrient dependencies for further clinical development, either by nutrient restriction or pathway inhibition. More recently, researchers have observed an increasingly strong linkage between altered mitochondrial Ca homeostasis and tumor cell metabolism, with strong implications for therapeutic targeting. In this review, we summarize the literature surrounding mitochondrial Ca homeostasis, metabolism, and cancer, as well as providing a discussion of the potential for mitochondrial Ca modulation as an anticancer therapeutic modality.
尽管在靶向小分子和免疫治疗干预方面取得了许多突破,但癌症仍是发达国家的主要死因。深入了解恶性肿瘤的特征和过程将使我们能够开发出更有效的治疗方案,以改善患者的治疗效果。一个特别感兴趣的领域是癌细胞代谢。早在20世纪20年代,奥托·瓦伯格就认识到癌细胞中代谢失调的现象。代谢改变可能通过营养限制或途径抑制为进一步的临床开发提供可靶向的营养依赖性。最近,研究人员观察到线粒体钙稳态改变与肿瘤细胞代谢之间的联系越来越紧密,这对治疗靶点具有重要意义。在这篇综述中,我们总结了围绕线粒体钙稳态、代谢和癌症的文献,并讨论了线粒体钙调节作为一种抗癌治疗方式的潜力。