Jiang Mingyang, Wang Jinlong, Li Yize, Zhang Ke, Wang Tao, Bo Zhandong, Lu Shenyi, Rodríguez Raquel Alarcón, Wei Ruqiong, Zhu Mingtao, Nicot Christophe, Sethi Gautam
Department of Bone and Joint Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Department of Neurosurgery, Binzhou Medical University Affiliated Shengli Oilfield Central Hospital, Dongying, China.
Drug Resist Updat. 2025 Jul 17;83:101276. doi: 10.1016/j.drup.2025.101276.
Cancer continues to be a primary cause of death, resulting in substantial mortality and illness globally. It remains a significant global health issue, greatly affecting morbidity and mortality across the world. Therapeutic resistance poses a major challenge to cancer treatments, acting as a significant barrier to the effectiveness of both standard and targeted therapies. This resistance develops through various mechanisms that allow tumor cells to adapt to and escape the damaging effects of chemotherapy, radiation, and targeted therapies. Ultimately, this leads to disease recurrence and progression. This review examines the dual roles of epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs) in promoting chemoresistance and metastasis. EMT is a dynamic and reversible biological process in which epithelial cells acquire mesenchymal characteristics, increasing their invasiveness and resistance to programmed cell death. CSCs are a subset of cancer cells with the ability to self-renew and play a crucial role in tumor relapse and resistance to treatment. EMT and CSCs are closely interconnected, collaboratively enhancing cancer cell plasticity, metastatic ability, and treatment resistance. The initiation of EMT in cancer cells can generate a CSC-like population, which promotes tumor recurrence and spread. This interaction highlights the importance of targeting both EMT and CSC pathways to develop more effective treatment strategies that address treatment resistance and prevent metastasis. Promising approaches include using natural substances, small molecules, and nanotechnology to block critical signaling pathways and interfere with resistance mechanisms. A more thorough understanding of the molecular factors underlying EMT and CSC plasticity is crucial for crafting personalized treatments that target tumor heterogeneity and improve clinical outcomes.
癌症仍然是主要的死亡原因,在全球范围内导致大量死亡和疾病。它仍然是一个重大的全球健康问题,极大地影响着世界各地的发病率和死亡率。治疗耐药性对癌症治疗构成了重大挑战,是标准疗法和靶向疗法有效性的重大障碍。这种耐药性通过各种机制产生,使肿瘤细胞能够适应并逃避化疗、放疗和靶向疗法的破坏作用。最终,这会导致疾病复发和进展。本综述探讨了上皮-间质转化(EMT)和癌症干细胞(CSC)在促进化疗耐药性和转移中的双重作用。EMT是一个动态且可逆的生物学过程,上皮细胞在此过程中获得间质特征,增加其侵袭性和对程序性细胞死亡的抗性。CSC是癌细胞的一个亚群,具有自我更新能力,在肿瘤复发和治疗耐药中起关键作用。EMT和CSC紧密相连,协同增强癌细胞的可塑性、转移能力和治疗耐药性。癌细胞中EMT的启动可产生类似CSC的细胞群,促进肿瘤复发和扩散。这种相互作用凸显了靶向EMT和CSC途径以制定更有效的治疗策略的重要性,这些策略可解决治疗耐药性并预防转移。有前景的方法包括使用天然物质、小分子和纳米技术来阻断关键信号通路并干扰耐药机制。更深入了解EMT和CSC可塑性背后的分子因素对于制定针对肿瘤异质性并改善临床结果的个性化治疗至关重要。