• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

转化生长因子β-1(TGFβ-1)诱导胰腺癌上皮-间质转化(EMT)过程中线粒体功能的变化

Changes in mitochondrial function during EMT induced by TGFβ-1 in pancreatic cancer.

作者信息

Guo Qingqu

机构信息

Department of Surgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, P.R. China.

出版信息

Oncol Lett. 2017 Mar;13(3):1575-1580. doi: 10.3892/ol.2017.5613. Epub 2017 Jan 18.

DOI:10.3892/ol.2017.5613
PMID:28454293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5403440/
Abstract

Mitochondrial dysfunction is linked to cancer. Differences in the number, morphology and function of mitochondria have been observed between normal cells and cancer cells. However, changes in mitochondrial function during epithelial-mesenchymal transition (EMT) in pancreatic cancer are less known. In the present study, the cultured human pancreatic cancer cell line Panc-1 was treated with transforming growth factor (TGF)β-1. Mitochondrial functions following TGFβ-1 exposure in pancreatic cancer were investigated. It was noticed that TGFβ-1 treatment induces morphologic changes and a shift from epithelial to mesenchymal phenotype in pancreatic cancer. Furthermore, increased mitochondrial mass was detected in pancreatic cancer following TGFβ-1 treatment. Besides, the production of reactive oxygen species in TGFβ-1-treated pancreatic cancer cells significantly increased compared with the control cells. Our results indicate that the phenomenon of EMT in pancreatic cancer has an association with mitochondrial dysfunction. Mitochondrial dysfunction may be a cause of EMT in pancreatic cancer, which leads to heterogeneity in pancreatic cancer, and may be a potential therapeutic target in the future.

摘要

线粒体功能障碍与癌症相关。正常细胞与癌细胞之间已观察到线粒体在数量、形态和功能上的差异。然而,胰腺癌上皮-间质转化(EMT)过程中线粒体功能的变化却鲜为人知。在本研究中,用转化生长因子(TGF)β-1处理培养的人胰腺癌细胞系Panc-1。研究了胰腺癌中TGFβ-1暴露后的线粒体功能。注意到TGFβ-1处理诱导了胰腺癌的形态变化以及从上皮表型向间质表型的转变。此外,TGFβ-1处理后的胰腺癌中线粒体质量增加。此外,与对照细胞相比,TGFβ-1处理的胰腺癌细胞中活性氧的产生显著增加。我们的结果表明,胰腺癌中的EMT现象与线粒体功能障碍有关。线粒体功能障碍可能是胰腺癌中EMT的一个原因,这导致了胰腺癌的异质性,并且可能是未来潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e13/5403440/441b25bf02f4/ol-13-03-1575-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e13/5403440/441b25bf02f4/ol-13-03-1575-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e13/5403440/441b25bf02f4/ol-13-03-1575-g02.jpg

相似文献

1
Changes in mitochondrial function during EMT induced by TGFβ-1 in pancreatic cancer.转化生长因子β-1(TGFβ-1)诱导胰腺癌上皮-间质转化(EMT)过程中线粒体功能的变化
Oncol Lett. 2017 Mar;13(3):1575-1580. doi: 10.3892/ol.2017.5613. Epub 2017 Jan 18.
2
TGFβ Signaling Increases Net Acid Extrusion, Proliferation and Invasion in Panc-1 Pancreatic Cancer Cells: SMAD4 Dependence and Link to Merlin/NF2 Signaling.转化生长因子β信号传导增加Panc-1胰腺癌细胞的净酸分泌、增殖和侵袭:SMAD4依赖性以及与Merlin/NF2信号传导的联系
Front Oncol. 2020 May 7;10:687. doi: 10.3389/fonc.2020.00687. eCollection 2020.
3
TGF Beta Induces Vitamin D Receptor and Modulates Mitochondrial Activity of Human Pancreatic Cancer Cells.转化生长因子β诱导维生素D受体并调节人胰腺癌细胞的线粒体活性。
Cancers (Basel). 2021 Jun 11;13(12):2932. doi: 10.3390/cancers13122932.
4
The Quasimesenchymal Pancreatic Ductal Epithelial Cell Line PANC-1-A Useful Model to Study Clonal Heterogeneity and EMT Subtype Shifting.准间充质胰腺导管上皮细胞系PANC-1——研究克隆异质性和上皮-间质转化亚型转变的有用模型
Cancers (Basel). 2022 Apr 19;14(9):2057. doi: 10.3390/cancers14092057.
5
Esophageal Adenocarcinoma Cells and Xenograft Tumors Exposed to Erb-b2 Receptor Tyrosine Kinase 2 and 3 Inhibitors Activate Transforming Growth Factor Beta Signaling, Which Induces Epithelial to Mesenchymal Transition.食管腺癌细胞和异种移植肿瘤暴露于表皮生长因子受体酪氨酸激酶 2 和 3 抑制剂可激活转化生长因子-β 信号通路,从而诱导上皮间质转化。
Gastroenterology. 2017 Jul;153(1):63-76.e14. doi: 10.1053/j.gastro.2017.03.004. Epub 2017 Mar 9.
6
Nox4-derived ROS signaling contributes to TGF-β-induced epithelial-mesenchymal transition in pancreatic cancer cells.Nox4 产生的 ROS 信号转导促进了胰腺癌细胞中 TGF-β诱导的上皮-间充质转化。
Anticancer Res. 2013 Oct;33(10):4431-8.
7
TGFβ Drives Metabolic Perturbations during Epithelial Mesenchymal Transition in Pancreatic Cancer: TGFβ Induced EMT in PDAC.转化生长因子β驱动胰腺癌上皮-间质转化过程中的代谢紊乱:转化生长因子β诱导胰腺导管腺癌发生上皮-间质转化
Cancers (Basel). 2021 Dec 9;13(24):6204. doi: 10.3390/cancers13246204.
8
Role of the integrin-linked kinase (ILK)/Rictor complex in TGFβ-1-induced epithelial-mesenchymal transition (EMT).整合素连接激酶 (ILK)/Rictor 复合物在 TGFβ-1 诱导的上皮-间充质转化 (EMT)中的作用。
Oncogene. 2013 Jan 3;32(1):50-60. doi: 10.1038/onc.2012.30. Epub 2012 Feb 6.
9
PARP3 controls TGFβ and ROS driven epithelial-to-mesenchymal transition and stemness by stimulating a TG2-Snail-E-cadherin axis.PARP3通过刺激转谷氨酰胺酶2-蜗牛-E-钙黏蛋白轴来控制转化生长因子β和活性氧驱动的上皮-间质转化及干性。
Oncotarget. 2016 Sep 27;7(39):64109-64123. doi: 10.18632/oncotarget.11627.
10
Monitoring Epithelial-Mesenchymal Transition of Pancreatic Cancer Cells via Investigation of Mitochondrial Dysfunction.通过研究线粒体功能障碍监测胰腺癌细胞的上皮-间质转化
Methods Protoc. 2020 Apr 27;3(2):32. doi: 10.3390/mps3020032.

引用本文的文献

1
Spatiotemporal Heterogeneity of Tumor Glucose Metabolism Reprogramming: From Single-Cell Mechanisms to Precision Interventions.肿瘤葡萄糖代谢重编程的时空异质性:从单细胞机制到精准干预
Int J Mol Sci. 2025 Jul 18;26(14):6901. doi: 10.3390/ijms26146901.
2
The Effect of Ionising Radiation on the Properties of Tumour-Derived Exosomes and Their Ability to Modify the Biology of Non-Irradiated Breast Cancer Cells-An In Vitro Study.电离辐射对肿瘤来源外泌体特性及其改变未受辐射乳腺癌细胞生物学特性能力的影响——一项体外研究
Int J Mol Sci. 2025 Jan 4;26(1):376. doi: 10.3390/ijms26010376.
3
Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition.

本文引用的文献

1
Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species.线粒体功能障碍通过增加活性氧的产生促进 HIF1α 积累,从而促进乳腺癌细胞迁移和侵袭。
PLoS One. 2013 Jul 29;8(7):e69485. doi: 10.1371/journal.pone.0069485. Print 2013.
2
Naringenin decreases invasiveness and metastasis by inhibiting TGF-β-induced epithelial to mesenchymal transition in pancreatic cancer cells.柚皮素通过抑制 TGF-β诱导的胰腺癌上皮间质转化而降低侵袭和转移。
PLoS One. 2012;7(12):e50956. doi: 10.1371/journal.pone.0050956. Epub 2012 Dec 26.
3
拓展视野:内皮-间充质转化的分子机制及疾病影响
Cell Commun Signal. 2025 Jan 9;23(1):16. doi: 10.1186/s12964-025-02028-y.
4
EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis.EPRS1介导的成纤维细胞活化和线粒体功能障碍促进肾纤维化。
Exp Mol Med. 2024 Dec;56(12):2673-2689. doi: 10.1038/s12276-024-01360-6. Epub 2024 Dec 2.
5
Biological and Clinical Impacts of Glucose Metabolism in Pancreatic Ductal Adenocarcinoma.葡萄糖代谢在胰腺导管腺癌中的生物学和临床影响
Cancers (Basel). 2023 Jan 13;15(2):498. doi: 10.3390/cancers15020498.
6
TGFβ Signaling in the Pancreatic Tumor Microenvironment.胰腺肿瘤微环境中的转化生长因子β信号传导
Cancers (Basel). 2021 Oct 11;13(20):5086. doi: 10.3390/cancers13205086.
7
Quantitative Proteomic Analysis in Alveolar Type II Cells Reveals the Different Capacities of RAS and TGF-β to Induce Epithelial-Mesenchymal Transition.II型肺泡细胞的定量蛋白质组学分析揭示了RAS和TGF-β诱导上皮-间质转化的不同能力。
Front Mol Biosci. 2021 Mar 19;8:595712. doi: 10.3389/fmolb.2021.595712. eCollection 2021.
8
Intrinsic and Extrinsic Modulators of the Epithelial to Mesenchymal Transition: Driving the Fate of Tumor Microenvironment.上皮-间质转化的内在和外在调节因子:驱动肿瘤微环境的命运
Front Oncol. 2020 Jul 24;10:1122. doi: 10.3389/fonc.2020.01122. eCollection 2020.
9
EMT signaling: potential contribution of CRISPR/Cas gene editing.EMT 信号转导:CRISPR/Cas 基因编辑的潜在贡献。
Cell Mol Life Sci. 2020 Jul;77(14):2701-2722. doi: 10.1007/s00018-020-03449-3. Epub 2020 Feb 1.
10
The enhancement of glycolysis regulates pancreatic cancer metastasis.糖酵解的增强调控胰腺癌转移。
Cell Mol Life Sci. 2020 Jan;77(2):305-321. doi: 10.1007/s00018-019-03278-z. Epub 2019 Aug 20.
Mitochondria as a source of reactive oxygen and nitrogen species: from molecular mechanisms to human health.
线粒体作为活性氧和氮物种的来源:从分子机制到人类健康。
Antioxid Redox Signal. 2013 Jun 1;18(16):2029-74. doi: 10.1089/ars.2012.4729. Epub 2013 Feb 19.
4
p21(WAF¹/C¹P¹) deficiency induces mitochondrial dysfunction in HCT116 colon cancer cells.p21(WAF1/CIP1) 缺失导致 HCT116 结肠癌细胞线粒体功能障碍。
Biochem Biophys Res Commun. 2013 Jan 11;430(2):653-8. doi: 10.1016/j.bbrc.2012.11.096. Epub 2012 Dec 2.
5
High mitochondrial DNA copy number and bioenergetic function are associated with tumor invasion of esophageal squamous cell carcinoma cell lines.高线粒体DNA拷贝数和生物能量功能与食管鳞状细胞癌细胞系的肿瘤侵袭相关。
Int J Mol Sci. 2012;13(9):11228-11246. doi: 10.3390/ijms130911228. Epub 2012 Sep 10.
6
Is mitochondrial DNA content a potential biomarker of mitochondrial dysfunction?线粒体 DNA 含量是否是线粒体功能障碍的潜在生物标志物?
Mitochondrion. 2013 Sep;13(5):481-92. doi: 10.1016/j.mito.2012.10.011. Epub 2012 Oct 22.
7
Deguelin suppresses pancreatic tumor growth and metastasis by inhibiting epithelial-to-mesenchymal transition in an orthotopic model.地榆苷通过抑制原位模型中的上皮间质转化抑制胰腺肿瘤生长和转移。
Oncogene. 2013 Aug 22;32(34):3980-91. doi: 10.1038/onc.2012.413. Epub 2012 Sep 17.
8
Mitochondrial dysfunction and cancer metastasis.线粒体功能障碍与癌症转移。
J Bioenerg Biomembr. 2012 Dec;44(6):619-22. doi: 10.1007/s10863-012-9465-9.
9
Pancreatic cancer cells enhance the ability of collagen internalization during epithelial-mesenchymal transition.胰腺癌细胞在上皮-间质转化过程中增强了胶原蛋白内化的能力。
PLoS One. 2012;7(7):e40434. doi: 10.1371/journal.pone.0040434. Epub 2012 Jul 5.
10
Rationale for mitochondria-targeting strategies in cancer bioenergetic therapies.癌症生物能量治疗中靶向线粒体策略的原理。
Int J Biochem Cell Biol. 2013 Jan;45(1):123-9. doi: 10.1016/j.biocel.2012.07.005. Epub 2012 Jul 7.