Tufail Muhammad
Department of Oral and Maxillofacial Surgery, Center of Stomatology, Xiangya Hospital, Central South University, Changsha, China.
Toxicol Rep. 2025 Mar 4;14:101987. doi: 10.1016/j.toxrep.2025.101987. eCollection 2025 Jun.
In cancer resistance, (PTEN) has emerged as a prominent protagonist. exerts its influence by regulating crucial signaling pathways that govern cell proliferation, survival, and differentiation. This comprehensive review article investigates deeply into the complex realm of -mediated drug resistance mechanisms in cancers. Our journey begins by exploring foundational role of PTEN, unveiling its significance as a molecular conductor that intricately coordinates vital cellular pathways. We thoroughly dissected the intricate milieu of alterations, including mutations, deletions, and epigenetic silencing, and elucidated their profound implications for fueling cancer growth and evading treatment. As we navigate the complex network of , we unravel the intricate interplay between and pivotal signaling pathways, such as PI3K/AKT, MAPK/ERK, and Wnt/β-catenin, further complicating the resistance landscape. This expedition, through these intricately intertwined signaling cascades, provides insight into the multifaceted mechanisms driving resistance, thereby revealing potential exploitable weaknesses. In our quest for therapeutic strategies, we need to explore innovative approaches to restore function, encompassing genetic therapies, pharmacological agents, and precision medicines tailored to status. The concept of combination therapy has emerged as a potent tool to overcome -associated resistance, offering promising synergistic interactions with standard treatments, targeted therapies, or immunotherapy. This review offers a comprehensive overview of -mediated drug resistance mechanisms in cancer and elucidates intricate interactions within this complex landscape. This underscores the central role of in drug resistance and provides valuable insights into promising strategies with the potential to reshape the future of cancer treatment.
在癌症耐药性方面,磷酸酶和张力蛋白同源物(PTEN)已成为一个重要的主角。它通过调节控制细胞增殖、存活和分化的关键信号通路来发挥作用。这篇全面的综述文章深入研究了PTEN介导的癌症耐药机制的复杂领域。我们的探索之旅始于探究PTEN的基础作用,揭示其作为精细协调重要细胞通路的分子导体的重要性。我们深入剖析了PTEN改变的复杂环境,包括突变、缺失和表观遗传沉默,并阐明了它们对促进癌症生长和逃避治疗的深远影响。当我们在PTEN的复杂网络中探寻时,我们揭示了PTEN与关键信号通路(如PI3K/AKT、MAPK/ERK和Wnt/β-连环蛋白)之间的复杂相互作用,这进一步使耐药情况复杂化。通过这些错综复杂的信号级联反应的探索,深入了解了驱动耐药性的多方面机制,从而揭示了潜在的可利用弱点。在寻求治疗策略的过程中,我们需要探索恢复PTEN功能的创新方法,包括基因疗法、药物制剂以及根据PTEN状态定制的精准药物。联合治疗的概念已成为克服与PTEN相关耐药性的有力工具,与标准治疗、靶向治疗或免疫治疗提供了有前景的协同相互作用。这篇综述全面概述了PTEN介导的癌症耐药机制,并阐明了这一复杂领域内的复杂相互作用。这突出了PTEN在耐药性中的核心作用,并为有可能重塑癌症治疗未来的有前景策略提供了有价值的见解。