Guo Yonggang, Morshedi Mohammadamin
Pingdingshan College, Pingdingshan, Henan, China.
School of Medicine, Kashan University of Medical Sciences, Kashan, Iran.
Front Bioeng Biotechnol. 2025 Mar 20;13:1547757. doi: 10.3389/fbioe.2025.1547757. eCollection 2025.
Zinc oxide nanoparticles (ZnO-NPs) have gained significant attention in cancer therapy due to their unique physical and chemical properties, particularly in treating gastrointestinal (GI) cancers such as gastric, colorectal, and hepatocellular carcinoma. These nanoparticles generate reactive oxygen species (ROS) upon entering cancer cells, causing oxidative stress that leads to cellular damage, DNA fragmentation, and apoptosis. ZnO-NPs affect the expression of key proteins involved in apoptosis, including p53, Bax, and Bcl-2, which regulate cell cycle arrest and programmed cell death. Additionally, ZnO-NPs can reduce mitochondrial membrane potential, further enhancing apoptosis in cancer cells. Furthermore, ZnO-NPs inhibit cancer cell proliferation by interfering with cell cycle progression. They reduce levels of cyclins and cyclin-dependent kinases (CDKs), leading to cell cycle arrest. ZnO-NPs also exhibit anti-metastatic properties by inhibiting the migration and invasion of cancer cells through modulation of signaling pathways that affect cell adhesion and cytoskeletal dynamics. The efficacy of ZnO-NPs in overcoming chemotherapy resistance has been demonstrated by their ability to reduce the IC50 values of chemotherapeutic agents, making cancer cells more susceptible to drug-induced cell death. In this review, we summarize the mechanisms by which ZnO-NPs exert anticancer effects in GI cancers, focusing on apoptosis, cell cycle regulation, and metastasis inhibition, while also highlighting the current limitations in translating these findings into effective clinical treatments.
氧化锌纳米颗粒(ZnO-NPs)因其独特的物理和化学性质在癌症治疗中受到了广泛关注,尤其是在治疗胃肠道(GI)癌症,如胃癌、结直肠癌和肝细胞癌方面。这些纳米颗粒进入癌细胞后会产生活性氧(ROS),引发氧化应激,导致细胞损伤、DNA片段化和细胞凋亡。ZnO-NPs会影响参与细胞凋亡的关键蛋白的表达,包括p53、Bax和Bcl-2,这些蛋白可调节细胞周期停滞和程序性细胞死亡。此外,ZnO-NPs可降低线粒体膜电位,进一步增强癌细胞的凋亡。此外,ZnO-NPs通过干扰细胞周期进程来抑制癌细胞增殖。它们会降低细胞周期蛋白和细胞周期蛋白依赖性激酶(CDK)的水平,导致细胞周期停滞。ZnO-NPs还通过调节影响细胞黏附和细胞骨架动力学的信号通路,抑制癌细胞的迁移和侵袭,从而表现出抗转移特性。ZnO-NPs降低化疗药物IC50值的能力证明了其克服化疗耐药性的功效,使癌细胞更容易受到药物诱导的细胞死亡。在这篇综述中,我们总结了ZnO-NPs在胃肠道癌症中发挥抗癌作用的机制,重点关注细胞凋亡、细胞周期调节和转移抑制,同时也强调了将这些研究结果转化为有效临床治疗方法目前存在的局限性。