收稿日期: 2025-04-16
网络出版日期: 2025-07-29
基金资助
国家自然科学基金项目(82074347)
Advances in the mechanism and therapeutic potential of Erianin⁃induced apoptosis in breast cancer cells
Received date: 2025-04-16
Online published: 2025-07-29
该综述系统探讨了来源于传统中药石斛的活性成分毛兰素在乳腺癌,尤其是三阴性乳腺癌(TNBC)治疗中的研究进展。作为缺乏雌激素受体(estrogen receptor, ER)、孕激素受体(PR)及人表皮生长因子受体2(HER2)表达的侵袭性亚型,TNBC因治疗靶点匮乏,治疗选择有限,临床仍主要依赖传统化疗方案。毛兰素通过诱导乳腺癌细胞凋亡展现了显著的抗癌潜力,其作用机制主要包括通过激活内源性和外源性凋亡途径,特别是线粒体功能紊乱介导的细胞色素c释放和半胱天冬酶(caspase)依赖性途径的激活,从而增强癌细胞对死亡信号的敏感性。在分子水平,毛兰素在调节磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/Akt)、丝裂原活化蛋白激酶(MAPK)和活化T细胞核因子1(NFATc1)等关键致癌通路方面表现出显著效果,能够抑制细胞增殖、迁移及诱导细胞凋亡。然而,尽管毛兰素具有良好的抗癌效果,其开发仍面临溶解度差和生物利用度低等挑战。因此,探索毛兰素与化疗药物的协同作用及作为放射增敏剂的潜力成为提升临床应用价值的重要研究方向。值得关注的是,毛兰素通过重塑凋亡调控网络(如调节Bax/Bcl-2蛋白比例)克服TNBC耐药性的独特优势,使其成为极具前景的多靶点治疗候选药物。目前大多数证据来自体外和动物实验,未来需通过人类临床试验进一步验证其疗效和安全性,并结合纳米递送系统优化、结构衍生物开发等策略改善药代动力学特性。本综述系统梳理毛兰素诱导凋亡的核心机制及治疗潜力,为开发针对TNBC的创新治疗方案提供理论依据。
李京朔 , 刘首诗 , 郭宏伟 . 毛兰素诱导乳腺癌细胞凋亡的机制及治疗潜力的研究进展[J]. 实用医学杂志, 2025 , 41(14) : 2132 -2137 . DOI: 10.3969/j.issn.1006-5725.2025.14.002
This review systematically elucidates recent advances in the therapeutic application of Erianin, a natural compound derived from Dendrobium, a traditional Chinese medicine, in the treatment of breast cancer, with particular emphasis on triple-negative breast cancer (TNBC). TNBC is characterized by the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression, which presents significant clinical challenges due to limited therapeutic targets and continued reliance on conventional chemotherapy. Erianin exhibits notable anticancer potential through the induction of apoptosis in breast cancer cells. Its primary mechanisms involve sensitizing cancer cells to apoptotic signals via activation of both intrinsic and extrinsic apoptotic pathways, particularly through mitochondrial dysfunction-mediated cytochrome c release and subsequent activation of caspase-dependent pathways. At the molecular level, Erianin effectively modulates key oncogenic signaling pathways, including PI3K/Akt, MAPK, and NFATc1 cascades, thereby suppressing cell proliferation and migration while promoting apoptosis. However, current research priorities center on investigating its synergistic effects with chemotherapeutic agents and assessing its radiosensitization potential to further enhance its clinical utility. Notably, Erianin demonstrates unique advantages in overcoming drug resistance in TNBC by modulating apoptotic regulatory networks, particularly through regulation of the Bax/Bcl-2 protein ratio, positioning it as a promising multi-target therapeutic candidate. Although existing evidence largely stems from in vitro and animal studies, future research should prioritize human clinical trials to validate its efficacy and safety, alongside pharmaceutical optimization strategies such as the development of nanodelivery systems and exploration of structural derivatives. This review systematically clarifies the core mechanism and therapeutic potential of pilanin-induced apoptosis, and provides theoretical basis for developing innovative therapeutic regimens for TNBC.
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