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探索鞣花酸在预防胃肠道癌症方面的潜力:最新进展与未来方向

Exploring the Potential of Ellagic Acid in Gastrointestinal Cancer Prevention: Recent Advances and Future Directions.

作者信息

Chauhan Abhishek, Yadav Monika, Chauhan Ritu, Basniwal Rupesh Kumar, Pathak Vinay Mohan, Ranjan Anuj, Kapardar Raj Kishor, Srivastav Rajpal, Tuli Hardeep Singh, Ramniwas Seema, Mathkor Darin Mansor, Haque Shafiul, Hussain Arif

机构信息

Amity Institute of Environmental Toxicology Safety and Management, Amity University, Noida, U.P., India.

Cancer Biology Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.

出版信息

Oncol Ther. 2024 Dec;12(4):685-699. doi: 10.1007/s40487-024-00296-1. Epub 2024 Sep 2.

DOI:10.1007/s40487-024-00296-1
PMID:39222186
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11574235/
Abstract

Gastrointestinal (GI) cancers are a significant global health concern with diverse etiologies and limited treatment options. Ellagic acid (EA), a natural polyphenolic compound, exhibits promising anticancer properties against various GI malignancies. In this article, we have reviewed recent research on the anticancer potential of EA across esophageal, gastric, colorectal, pancreatic, and liver cancers. In esophageal cancer, EA inhibits the formation of O6-methylguanine (O6-meGua) adducts induced by carcinogens like N-nitrosomethylbenzylamine (NMBA), thereby suppressing tumor growth. Additionally, EA inhibits STAT3 signaling and stabilizes tumor suppressor proteins, showing potential as an anti-esophageal cancer agent. In gastric cancer, EA regulates multiple pathways involved in cell proliferation, invasion, and apoptosis, including the p53 and PI3K-Akt signaling pathways. It also demonstrates anti-inflammatory and antioxidant effects, making it a promising therapeutic candidate against gastric cancer. In colorectal cancer (CRC), EA inhibits cell proliferation, induces apoptosis, and modulates the Wnt/β-catenin and PI3K/Akt pathways, suggesting its efficacy in preventing CRC progression. Furthermore, EA has shown promise in pancreatic cancer by inhibiting nuclear factor-kappa B, inducing apoptosis, and suppressing epithelial-mesenchymal transition. In liver cancer, EA exhibits radio-sensitizing effects, inhibits inflammatory pathways, and modulates the tumor microenvironment, offering potential therapeutic benefits against hepatocellular carcinoma. Studies on EA potential in combination therapies and the development of targeted delivery systems are required for enhanced efficacy against gastrointestinal cancers.

摘要

胃肠道(GI)癌症是一个重大的全球健康问题,其病因多样且治疗选择有限。鞣花酸(EA)是一种天然多酚化合物,对各种胃肠道恶性肿瘤具有有前景的抗癌特性。在本文中,我们综述了EA在食管癌、胃癌、结直肠癌、胰腺癌和肝癌抗癌潜力方面的最新研究。在食管癌中,EA抑制由N-亚硝基甲基苄胺(NMBA)等致癌物诱导的O6-甲基鸟嘌呤(O6-meGua)加合物的形成,从而抑制肿瘤生长。此外,EA抑制信号转导和转录激活因子3(STAT3)信号传导并稳定肿瘤抑制蛋白,显示出作为抗食管癌药物的潜力。在胃癌中,EA调节参与细胞增殖、侵袭和凋亡的多种途径,包括p53和磷脂酰肌醇-3-激酶/蛋白激酶B(PI3K-Akt)信号通路。它还表现出抗炎和抗氧化作用,使其成为对抗胃癌的有前景的治疗候选物。在结直肠癌(CRC)中,EA抑制细胞增殖、诱导凋亡并调节Wnt/β-连环蛋白和PI3K/Akt途径,表明其在预防CRC进展方面的功效。此外,EA通过抑制核因子-κB、诱导凋亡和抑制上皮-间质转化在胰腺癌中显示出前景。在肝癌中,EA表现出放射增敏作用,抑制炎症途径并调节肿瘤微环境,为肝细胞癌提供潜在的治疗益处。为了提高对胃肠道癌症的疗效,需要对EA在联合治疗中的潜力以及靶向递送系统的开发进行研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e2/11574235/56fb44454847/40487_2024_296_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e2/11574235/5334d025444c/40487_2024_296_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e2/11574235/56fb44454847/40487_2024_296_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e2/11574235/5334d025444c/40487_2024_296_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e2/11574235/56fb44454847/40487_2024_296_Fig2_HTML.jpg

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本文引用的文献

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CA Cancer J Clin. 2024 May-Jun;74(3):229-263. doi: 10.3322/caac.21834. Epub 2024 Apr 4.
2
Integrating natural compounds and nanoparticle-based drug delivery systems: A novel strategy for enhanced efficacy and selectivity in cancer therapy.整合天然化合物和基于纳米粒子的药物传递系统:提高癌症治疗疗效和选择性的新策略。
Cancer Med. 2024 Mar;13(5):e7010. doi: 10.1002/cam4.7010.
3
Oral administration of ellagic acid mitigates perioperative neurocognitive disorders, hippocampal oxidative stress, and neuroinflammation in aged mice by restoring IGF-1 signaling.
口服鞣花酸通过恢复 IGF-1 信号减轻老年小鼠围手术期神经认知障碍、海马氧化应激和神经炎症。
Sci Rep. 2024 Jan 30;14(1):2509. doi: 10.1038/s41598-024-53127-8.
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Dishevelled-associated antagonist of β-catenin homolog 3 (DACT3) suppresses glioma progression though Notch1 signaling pathway in β-catenin-dependent manner.β-连环蛋白同源物3的蓬乱相关拮抗剂(DACT3)通过Notch1信号通路以β-连环蛋白依赖性方式抑制胶质瘤进展。
Heliyon. 2023 Dec 27;10(1):e23511. doi: 10.1016/j.heliyon.2023.e23511. eCollection 2024 Jan 15.
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Curr Med Chem. 2024;31(32):5199-5221. doi: 10.2174/0109298673275501231213063902.
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