Suppr超能文献

活性氧与胰腺癌的靶向治疗

Reactive Oxygen Species and Targeted Therapy for Pancreatic Cancer.

作者信息

Zhang Lun, Li Jiahui, Zong Liang, Chen Xin, Chen Ke, Jiang Zhengdong, Nan Ligang, Li Xuqi, Li Wei, Shan Tao, Ma Qingyong, Ma Zhenhua

机构信息

Department of Hepatobiliary Surgery, First Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710061, China.

Department of General Surgery, First Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710061, China.

出版信息

Oxid Med Cell Longev. 2016;2016:1616781. doi: 10.1155/2016/1616781. Epub 2016 Jan 3.

Abstract

Pancreatic cancer is the fourth leading cause of cancer-related death in the United States. Reactive oxygen species (ROS) are generally increased in pancreatic cancer cells compared with normal cells. ROS plays a vital role in various cellular biological activities including proliferation, growth, apoptosis, and invasion. Besides, ROS participates in tumor microenvironment orchestration. The role of ROS is a doubled-edged sword in pancreatic cancer. The dual roles of ROS depend on the concentration. ROS facilitates carcinogenesis and cancer progression with mild-to-moderate elevated levels, while excessive ROS damages cancer cells dramatically and leads to cell death. Based on the recent knowledge, either promoting ROS generation to increase the concentration of ROS with extremely high levels or enhancing ROS scavenging ability to decrease ROS levels may benefit the treatment of pancreatic cancer. However, when faced with oxidative stress, the antioxidant programs of cancer cells have been activated to help cancer cells to survive in the adverse condition. Furthermore, ROS signaling and antioxidant programs play the vital roles in the progression of pancreatic cancer and in the response to cancer treatment. Eventually, it may be the novel target for various strategies and drugs to modulate ROS levels in pancreatic cancer therapy.

摘要

胰腺癌是美国癌症相关死亡的第四大主要原因。与正常细胞相比,胰腺癌细胞中的活性氧(ROS)通常会增加。ROS在包括增殖、生长、凋亡和侵袭在内的各种细胞生物学活动中起着至关重要的作用。此外,ROS参与肿瘤微环境的调控。ROS在胰腺癌中扮演着双刃剑的角色。ROS的双重作用取决于其浓度。ROS在轻度至中度升高水平时促进致癌作用和癌症进展,而过量的ROS会显著损害癌细胞并导致细胞死亡。基于最近的认识,促进ROS生成以增加ROS浓度至极高水平或增强ROS清除能力以降低ROS水平可能有利于胰腺癌的治疗。然而,当面对氧化应激时,癌细胞的抗氧化程序已被激活,以帮助癌细胞在不利条件下存活。此外,ROS信号传导和抗氧化程序在胰腺癌的进展以及对癌症治疗的反应中起着至关重要的作用。最终,调节胰腺癌治疗中ROS水平可能成为各种策略和药物的新靶点。

相似文献

1
Reactive Oxygen Species and Targeted Therapy for Pancreatic Cancer.
Oxid Med Cell Longev. 2016;2016:1616781. doi: 10.1155/2016/1616781. Epub 2016 Jan 3.
2
Design and discovery of novel quinazolinedione-based redox modulators as therapies for pancreatic cancer.
Biochim Biophys Acta. 2014 Jan;1840(1):332-43. doi: 10.1016/j.bbagen.2013.08.005. Epub 2013 Aug 15.
3
Free radicals, metals and antioxidants in oxidative stress-induced cancer.
Chem Biol Interact. 2006 Mar 10;160(1):1-40. doi: 10.1016/j.cbi.2005.12.009. Epub 2006 Jan 23.
4
Redox Homeostasis and Cellular Antioxidant Systems: Crucial Players in Cancer Growth and Therapy.
Oxid Med Cell Longev. 2016;2016:6235641. doi: 10.1155/2016/6235641. Epub 2016 Jun 21.
5
"Double-edged sword" effect of reactive oxygen species (ROS) in tumor development and carcinogenesis.
Physiol Res. 2023 Jul 14;72(3):301-307. doi: 10.33549/physiolres.935007.
6
Reactive oxygen species in redox cancer therapy.
Cancer Lett. 2015 Oct 10;367(1):18-25. doi: 10.1016/j.canlet.2015.07.008. Epub 2015 Jul 14.
7
KRas, ROS and the initiation of pancreatic cancer.
Small GTPases. 2017 Jan 2;8(1):38-42. doi: 10.1080/21541248.2016.1192714. Epub 2016 May 24.
9
Reactive oxygen species and colorectal cancer.
J Cell Physiol. 2018 Jul;233(7):5119-5132. doi: 10.1002/jcp.26356. Epub 2018 Jan 25.
10
Targeting Redox Metabolism in Pancreatic Cancer.
Int J Mol Sci. 2021 Feb 3;22(4):1534. doi: 10.3390/ijms22041534.

引用本文的文献

1
and drive metabolic reprogramming in pancreatic cancer cells: the influence of oxidative and nitrosatice stress.
Front Cell Dev Biol. 2025 Jun 11;13:1547582. doi: 10.3389/fcell.2025.1547582. eCollection 2025.
7
Nimbolide: A Potential Phytochemical Agent in Multimodal Pancreatic Cancer Therapies.
Mini Rev Med Chem. 2025;25(1):27-41. doi: 10.2174/0113895575293138240527061556.
8
Molecular mechanisms underlying methotrexate-induced intestinal injury and protective strategies.
Naunyn Schmiedebergs Arch Pharmacol. 2024 Nov;397(11):8165-8188. doi: 10.1007/s00210-024-03164-x. Epub 2024 Jun 1.
9
Pan-cancer analysis of the interplay between mutational signatures and cellular signaling.
iScience. 2024 May 2;27(6):109873. doi: 10.1016/j.isci.2024.109873. eCollection 2024 Jun 21.
10
The bacterial metabolite, lithocholic acid, has antineoplastic effects in pancreatic adenocarcinoma.
Cell Death Discov. 2024 May 23;10(1):248. doi: 10.1038/s41420-024-02023-1.

本文引用的文献

3
Longikaurin E induces apoptosis of pancreatic cancer cells via modulation of the p38 and PI3K/AKT pathways by ROS.
Naunyn Schmiedebergs Arch Pharmacol. 2015 Jun;388(6):623-34. doi: 10.1007/s00210-015-1107-4. Epub 2015 Mar 6.
4
Gemcitabine-induced CXCL8 expression counteracts its actions by inducing tumor neovascularization.
Biochem Biophys Res Commun. 2015 Mar 6;458(2):341-6. doi: 10.1016/j.bbrc.2015.01.112. Epub 2015 Jan 31.
5
ROS and energy metabolism in cancer cells: alliance for fast growth.
Arch Pharm Res. 2015 Mar;38(3):338-45. doi: 10.1007/s12272-015-0550-6. Epub 2015 Jan 20.
6
Onconase induces autophagy sensitizing pancreatic cancer cells to gemcitabine and activates Akt/mTOR pathway in a ROS-dependent manner.
Biochim Biophys Acta. 2015 Mar;1853(3):549-60. doi: 10.1016/j.bbamcr.2014.12.016. Epub 2014 Dec 20.
7
Mechanisms of Overcoming Intrinsic Resistance to Gemcitabine in Pancreatic Ductal Adenocarcinoma through the Redox Modulation.
Mol Cancer Ther. 2015 Mar;14(3):788-98. doi: 10.1158/1535-7163.MCT-14-0420. Epub 2014 Dec 19.
10
Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles' heel?
Nat Rev Cancer. 2014 Nov;14(11):709-21. doi: 10.1038/nrc3803.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验