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从动态角度重新审视黄连素在预防和治疗诱导性结直肠癌中的作用。

Revisiting berberine for the prevention and treatment of -induced colorectal cancer from a dynamic perspective.

作者信息

Bi Dongming, Yang Xue, Yong Jiangyan, Huang Ju, Liu Zhihao, Gong Rui

机构信息

Department of Laboratory Medicine, Chengdu University of Traditional Chinese Medicine Hospital, Chengdu, Sichuan, China.

Department of laboratory Medicine. Deyang Hospital Affiliated Hospital of Chengdu University of Traditional Chinese Medicine, Deyang, Sichuan, China.

出版信息

Front Microbiol. 2025 Sep 11;16:1637272. doi: 10.3389/fmicb.2025.1637272. eCollection 2025.

DOI:10.3389/fmicb.2025.1637272
PMID:41019530
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12461290/
Abstract

Colorectal Cancer (CRC), a common malignancy, often arises from adenomatous precursors. In the adenoma-carcinoma progression of CRC, (Fn) plays an important driving role. Therefore, the discovery of new drugs targeting Fn-induced disease progression is crucial for the prevention and treatment of CRC. Berberine (BBR), which has a relatively broad spectrum of antitumor activity, has received increasing attention in recent years. In this study, we summarize BBR's regulatory effects on the different stages of intestinal adenoma-carcinoma transformation induced by Fn and its anti-tumor mechanisms in the occurrence and development of CRC for the first time. Firstly, BBR can prevent the migration and intestinal colonization of Fn and regulate Fn-induced microbiota imbalance. Secondly, in the pre-cancerous lesion stage, BBR can attenuates Fn-mediated inflammation, inhibit abnormal crypt foci, and reverse adenoma progression. In addition, BBR can suppresses established CRC by inhibiting cell proliferation, invasion, metastasis, immune escape and drug resistance. For the classic pathogenic model of Fn-mediated CRC, the therapeutic effect of BBR is dynamic and comprehensive from pathogenic factors to pathological products. Among them, E-cadherin, Wnt/β-catenin, JAK/STAT and MAPK/ERK signaling pathways may be key to BBR's prevention of Fn-induced CRC.

摘要

结直肠癌(CRC)是一种常见的恶性肿瘤,通常起源于腺瘤性前体。在CRC的腺瘤-癌进展过程中,(Fn)发挥着重要的驱动作用。因此,发现针对Fn诱导的疾病进展的新药对于CRC的预防和治疗至关重要。黄连素(BBR)具有相对广泛的抗肿瘤活性,近年来受到越来越多的关注。在本研究中,我们首次总结了BBR对Fn诱导的肠道腺瘤-癌转化不同阶段的调节作用及其在CRC发生发展中的抗肿瘤机制。首先,BBR可以阻止Fn的迁移和肠道定植,并调节Fn诱导的微生物群失衡。其次,在癌前病变阶段,BBR可以减轻Fn介导的炎症,抑制异常隐窝灶,并逆转腺瘤进展。此外,BBR可以通过抑制细胞增殖、侵袭、转移、免疫逃逸和耐药性来抑制已形成的CRC。对于Fn介导的CRC经典致病模型,BBR的治疗作用从致病因素到病理产物是动态且全面的。其中,E-钙黏蛋白、Wnt/β-连环蛋白、JAK/STAT和MAPK/ERK信号通路可能是BBR预防Fn诱导的CRC的关键。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/fa590b134c0d/fmicb-16-1637272-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/a7d9d7cd01b6/fmicb-16-1637272-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/d6c0e8166d4b/fmicb-16-1637272-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/4f7f7fad9bf8/fmicb-16-1637272-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/728659884b3f/fmicb-16-1637272-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/fa590b134c0d/fmicb-16-1637272-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/a7d9d7cd01b6/fmicb-16-1637272-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/d6c0e8166d4b/fmicb-16-1637272-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/4f7f7fad9bf8/fmicb-16-1637272-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/728659884b3f/fmicb-16-1637272-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cac4/12461290/fa590b134c0d/fmicb-16-1637272-g0005.jpg

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