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过氧化物酶体增殖物激活受体(PPAR)在结直肠癌中的调节作用。

Regulatory role of PPAR in colorectal cancer.

作者信息

Wang Cong, Lv Tingcong, Jin Binghui, Li Yang, Fan Zhe

机构信息

Department of General Surgery, The Third People's Hospital of Dalian, Dalian Medical University, Dalian, China.

Department of General Surgery, The Third People's Hospital of Dalian, Faculty of Medicine, Dalian University of Technology, Dalian, China.

出版信息

Cell Death Discov. 2025 Jan 28;11(1):28. doi: 10.1038/s41420-025-02313-2.

DOI:10.1038/s41420-025-02313-2
PMID:39875357
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11775197/
Abstract

Colorectal cancer (CRC) is one of the most common tumors in the digestive system, and the majority of patients are found to be in advanced stages, which is a burden to human health all over the world. Moreover, in recent years, CRC has been progressively becoming younger, with an increasing incidence mainly among patients <50 years old. Despite the increase in awareness of CRC and the continuous improvement of medical treatment nowadays, the challenge of CRC still needs to be conquered. By now, the pathogenesis of CRC is complex and not fully understood. With the deepening of research, it has been revealed that PPARs, as a transcription factor, are inextricably linked to CRC. This article outlines the mechanisms by which PPARs are involved in CRC development. An in-depth understanding of the pathways related to PPARs may provide new ways of developing effective therapies for CRC with PPARs as potential targets.

摘要

结直肠癌(CRC)是消化系统最常见的肿瘤之一,大多数患者确诊时已处于晚期,这给全球人类健康带来了负担。此外,近年来,CRC发病呈年轻化趋势,发病率上升主要集中在50岁以下的患者中。尽管目前人们对CRC的认识有所提高,医疗水平也在不断改善,但CRC带来的挑战仍有待攻克。到目前为止,CRC的发病机制复杂,尚未完全明确。随着研究的深入,发现过氧化物酶体增殖物激活受体(PPARs)作为一种转录因子,与CRC有着千丝万缕的联系。本文概述了PPARs参与CRC发生发展的机制。深入了解与PPARs相关的信号通路,可能为以PPARs为潜在靶点开发有效的CRC治疗方法提供新途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea6c/11775197/b47a4ec52662/41420_2025_2313_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea6c/11775197/6271273feb5a/41420_2025_2313_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea6c/11775197/57fb6c33da91/41420_2025_2313_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea6c/11775197/b47a4ec52662/41420_2025_2313_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea6c/11775197/6271273feb5a/41420_2025_2313_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea6c/11775197/57fb6c33da91/41420_2025_2313_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea6c/11775197/b47a4ec52662/41420_2025_2313_Fig3_HTML.jpg

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Vitexicarpin suppresses malignant progression of colorectal cancer through affecting c-Myc ubiquitination by targeting IMPDH2.牡荆素通过靶向肌苷酸脱氢酶2(IMPDH2)影响c-Myc泛素化,从而抑制结直肠癌的恶性进展。
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