Epigenetic changes regulate gene expression through histone modifications, chromatin remodeling, and protein translation of these modifications. The PRC1 and PRC2 complexes shape gene repression via histone modifications. Specifically, the CBX protein family aids PRC1 recruitment to chromatin, impacting the progressive multistep process driving chromatin silencing. Among family members, CBX3 is a complex protein involved in aberrant epigenetic mechanisms that drive lung cancer progression. CBX3 promotes lung tumorigenesis by interacting with key pathways such as PI3K/AKT, Ras/KRAS, Wnt/β-catenin, MAPK, Notch, and p53, leading to increased proliferation, inhibition of apoptosis, and enhanced resistance to therapy. Given our current lack of knowledge, additional research is required to uncover the intricate mechanisms underlying CBX3 activity, as well as its involvement in molecular pathways and its potential biomarker evaluation. Specifically, the dissimilar roles of CBX3 could be reexamined to gain a greater insight into lung cancer pathogenesis. This review aims to provide a clear overview of the context-related molecular profile of CBX3, which could be useful for addressing clinical challenges and developing novel targeted therapies based on personalized medicine.
表观遗传变化通过组蛋白修饰、染色质重塑以及这些修饰的蛋白质翻译来调控基因表达。PRC1和PRC2复合物通过组蛋白修饰介导基因抑制。具体而言，CBX蛋白家族协助PRC1募集至染色质，影响驱动染色质沉默的渐进多步骤过程。在家族成员中，CBX3是一种参与异常表观遗传机制的复杂蛋白，可驱动肺癌进展。CBX3通过与PI3K/AKT、Ras/KRAS、Wnt/β-catenin、MAPK、Notch及p53等关键通路相互作用，促进肺肿瘤发生，导致增殖增加、凋亡抑制及治疗耐受性增强。鉴于目前认知尚不充分，需要进一步研究以揭示CBX3活性的复杂机制、其在分子通路中的作用及其作为生物标志物的潜在价值。特别是，重新审视CBX3的差异化功能有助于更深入理解肺癌发病机制。本综述旨在系统阐述CBX3的情境依赖性分子特征，为应对临床挑战及开发基于个性化医疗的新型靶向疗法提供参考。
Exploring the Role of CBX3 as a Potential Therapeutic Target in Lung Cancer
肿瘤(癌症)患者之家