Tan Ee Wern, Singh Sachin Kumar, Dua Kamal, Gupta Gaurav, Lee Wai Leng, Wong Rebecca Shin Yee, Tan Kuan Onn, Goh Bey Hing
Sunway Biofunctional Molecules Discovery Centre, Faculty of Medical and Life Sciences, Sunway University, No. 5 Jalan Universiti, Petaling Jaya, Selangor Darul Ehsan, 47500, Malaysia.
School of Pharmaceutical Sciences, Lovely Professional University, Jalandhar - Delhi, Grand Trunk Rd, Phagwara, Punjab, 144411, India.
Mol Biol Rep. 2025 Jul 3;52(1):671. doi: 10.1007/s11033-025-10748-0.
Cancer stem cells (CSCs) play a critical role in tumor initiation, progression, and resistance to therapy, making them a major hurdle in effective cancer treatment. Unlike bulk cancer cells, CSCs exhibit remarkable adaptability, allowing them to survive under metabolic stress and evade conventional therapies. Mitochondria, as central regulators of cellular metabolism and apoptosis, are integral to CSC function. They facilitate metabolic reprogramming, redox balance, and stress adaptation, thereby enhancing CSC survival, self-renewal, and resistance to treatment. Dysregulated mitochondrial dynamics, including alterations in biogenesis, degradation, and signaling pathways, contribute to CSC maintenance and therapeutic resistance. Furthermore, mitochondrial membrane integrity and oxidative stress regulation determine CSC fate, influencing their ability to withstand chemotherapy and radiotherapy. Recent advances have identified mitochondrial-targeted strategies as promising approaches to impair CSC function and sensitize them to treatment. These include disrupting mitochondrial metabolism, inducing oxidative stress, and modulating mitochondrial quality control mechanisms. By understanding the intricate relationship between mitochondria and CSCs, new therapeutic strategies can be developed to selectively target CSCs, ultimately improving cancer treatment outcomes and preventing disease recurrence. This review provides an in-depth analysis of mitochondrial mechanisms in CSCs and their potential as therapeutic targets.
癌症干细胞(CSCs)在肿瘤的起始、进展以及对治疗的抗性中发挥着关键作用,这使得它们成为有效癌症治疗的主要障碍。与大多数癌细胞不同,癌症干细胞表现出显著的适应性,使其能够在代谢应激下存活并逃避传统疗法。线粒体作为细胞代谢和细胞凋亡的核心调节因子,对于癌症干细胞的功能至关重要。它们促进代谢重编程、氧化还原平衡和应激适应,从而增强癌症干细胞的存活、自我更新和对治疗的抗性。线粒体动力学失调,包括生物发生、降解和信号通路的改变,有助于癌症干细胞的维持和治疗抗性。此外,线粒体膜完整性和氧化应激调节决定了癌症干细胞的命运,影响它们耐受化疗和放疗的能力。最近的进展已将线粒体靶向策略确定为损害癌症干细胞功能并使其对治疗敏感的有前景的方法。这些策略包括破坏线粒体代谢、诱导氧化应激以及调节线粒体质量控制机制。通过了解线粒体与癌症干细胞之间的复杂关系,可以开发新的治疗策略来选择性地靶向癌症干细胞,最终改善癌症治疗效果并预防疾病复发。本综述对癌症干细胞中的线粒体机制及其作为治疗靶点的潜力进行了深入分析。