• 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-βI通过多能转录因子OCT4调控子宫内膜异位症中的细胞迁移。

TGF-βI Regulates Cell Migration through Pluripotent Transcription Factor OCT4 in Endometriosis.

作者信息

Au Heng-Kien, Chang Jui-Hung, Wu Yu-Chih, Kuo Yung-Che, Chen Yu-Hsi, Lee Wei-Chin, Chang Te-Sheng, Lan Pei-Chi, Kuo Hung-Chih, Lee Kha-Liang, Lee Mei-Tsu, Tzeng Chii-Ruey, Huang Yen-Hua

机构信息

Department of Obstetrics and Gynecology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Center for Reproductive Medicine, Taipei Medical University Hospital, Taipei Medical University, Taipei, Taiwan.

出版信息

PLoS One. 2015 Dec 16;10(12):e0145256. doi: 10.1371/journal.pone.0145256. eCollection 2015.

DOI:10.1371/journal.pone.0145256
PMID:26675296
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4682958/
Abstract

Transforming growth factor (TGF-β)/TGF-β receptor signal is known to promote cell migration. Up-regulation of TGF-β in serum/peritoneal fluid and increased levels of pluripotent transcription factor OCT4 in endometriotic tissues are frequently observed in patients with endometriosis. However, the mechanisms underlying how TGF-β/TGF-β receptor and OCT4 affect endometriotic cell migration still remain largely unknown. Therefore, endometriotic tissue with high cell migratory capacity were collected from patients with adenomyotic myometrium (n = 23) and chocolate cyst (n = 24); and endometrial tissue with low cell migratory capacity in normal endometrium or hyperplastic endometrium (n = 8) were collected as the controls. We found the mRNA levels of TGF-β receptor I (TGF-β RI) and OCT4 were significantly higher in the high-migratory ectopic endometriotic tissues than those of the low-migratory normal or hyperplastic endometrium. Positive correlations between TGF-β RI and OCT4, and either TGF-β RI or OCT4 with migration-related genes (SNAIL, SLUG and TWIST) regarding the mRNA levels were observed in human endometriotic tissues. TGF-βI dose-dependently increased the gene and protein levels of OCT4, SNAIL and N-Cadherin (N-CAD) and silencing of endogenous OCT4 significantly suppressed the TGF-βI-induced expressions of N-CAD and SNAIL in primary human endometriotic stromal cells and human endometrial carcinoma cell lines RL95-2 and HEC1A. Furthermore, TGF-βI significantly increased the migration ability of endometriotic cells and silencing of OCT4 dramatically suppressed the TGF-βI-induced cell migration activity evidenced by wound-closure assay, transwell assay, and confocal image of F-actin cellular distribution. In conclusion, the present findings demonstrate that the niche TGF-β plays a critical role in initiating expressions of pluripotent transcription factor OCT4 which may contribute to the ectopic endometrial growth by stimulating endometrial cell migration. These findings would be useful for developing therapeutic strategies targeting TGF-β-OCT4 signaling to prevent endometriosis in the future.

摘要

已知转化生长因子（TGF-β）/TGF-β受体信号可促进细胞迁移。子宫内膜异位症患者血清/腹腔液中TGF-β上调以及异位内膜组织中多能转录因子OCT4水平升高的情况屡见不鲜。然而，TGF-β/TGF-β受体与OCT4如何影响异位内膜细胞迁移的机制仍大多未知。因此，从子宫腺肌病肌层患者（n = 23）和巧克力囊肿患者（n = 24）中收集具有高细胞迁移能力的异位内膜组织；并收集正常子宫内膜或增生性子宫内膜中具有低细胞迁移能力的内膜组织（n = 8）作为对照。我们发现，高迁移性异位内膜组织中TGF-β受体I（TGF-β RI）和OCT4的mRNA水平显著高于低迁移性正常或增生性内膜组织。在人异位内膜组织中，观察到TGF-β RI与OCT4之间以及TGF-β RI或OCT4与迁移相关基因（SNAIL、SLUG和TWIST）的mRNA水平呈正相关。TGF-βI剂量依赖性地增加了OCT4、SNAIL和N-钙黏蛋白（N-CAD）的基因和蛋白水平，并且内源性OCT4的沉默显著抑制了TGF-βI诱导的原代人异位内膜基质细胞以及人子宫内膜癌细胞系RL95-2和HEC1A中N-CAD和SNAIL的表达。此外，TGF-βI显著增加了异位内膜细胞的迁移能力，而OCT4的沉默显著抑制了TGF-βI诱导的细胞迁移活性，这通过伤口愈合试验、Transwell试验以及F-肌动蛋白细胞分布的共聚焦图像得以证明。总之，本研究结果表明，局部的TGF-β在启动多能转录因子OCT4的表达中起关键作用，OCT4可能通过刺激内膜细胞迁移促进异位内膜生长。这些发现将有助于未来开发针对TGF-β - OCT4信号通路的治疗策略以预防子宫内膜异位症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff5/4682958/57d1483f95f5/pone.0145256.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff5/4682958/81cc970a44fe/pone.0145256.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff5/4682958/13a2da000b70/pone.0145256.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff5/4682958/43b866e58fdd/pone.0145256.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff5/4682958/57d1483f95f5/pone.0145256.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff5/4682958/81cc970a44fe/pone.0145256.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff5/4682958/13a2da000b70/pone.0145256.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff5/4682958/43b866e58fdd/pone.0145256.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff5/4682958/57d1483f95f5/pone.0145256.g004.jpg

相似文献

1
TGF-βI Regulates Cell Migration through Pluripotent Transcription Factor OCT4 in Endometriosis.转化生长因子-βI通过多能转录因子OCT4调控子宫内膜异位症中的细胞迁移。
PLoS One. 2015 Dec 16;10(12):e0145256. doi: 10.1371/journal.pone.0145256. eCollection 2015.
2
Expression of the pluripotent transcription factor OCT4 promotes cell migration in endometriosis.多能转录因子 OCT4 的表达促进子宫内膜异位症中的细胞迁移。
Fertil Steril. 2013 Apr;99(5):1332-1339.e5. doi: 10.1016/j.fertnstert.2012.11.033. Epub 2013 Jan 3.
3
Enhanced expression of the stemness-related factors OCT4, SOX15 and TWIST1 in ectopic endometrium of endometriosis patients.子宫内膜异位症患者异位内膜中干性相关因子OCT4、SOX15和TWIST1的表达增强。
Reprod Biol Endocrinol. 2016 Nov 24;14(1):81. doi: 10.1186/s12958-016-0215-4.
4
Enhanced epithelial to mesenchymal transition (EMT) and upregulated MYC in ectopic lesions contribute independently to endometriosis.异位病灶中增强的上皮-间质转化（EMT）和上调的MYC各自独立地促进子宫内膜异位症。
Reprod Biol Endocrinol. 2015 Jul 22;13:75. doi: 10.1186/s12958-015-0063-7.
5
Epithelial to mesenchymal transition (EMT) seems to be regulated differently in endometriosis and the endometrium.上皮间质转化（EMT）似乎在子宫内膜异位症和子宫内膜中受到不同的调控。
Arch Gynecol Obstet. 2014 Apr;289(4):871-81. doi: 10.1007/s00404-013-3040-4. Epub 2013 Oct 30.
6
Knockdown of vascular cell adhesion molecule 1 impedes transforming growth factor beta 1-mediated proliferation, migration, and invasion of endometriotic cyst stromal cells.敲低血管细胞黏附分子 1 可抑制转化生长因子 β1 介导的子宫内膜异位症囊肿间质细胞的增殖、迁移和侵袭。
Reprod Biol Endocrinol. 2019 Aug 23;17(1):69. doi: 10.1186/s12958-019-0512-9.
7
Roles of cell migration and invasion mediated by Twist in endometriosis.Twist介导的细胞迁移和侵袭在子宫内膜异位症中的作用。
J Obstet Gynaecol Res. 2019 Aug;45(8):1488-1496. doi: 10.1111/jog.14001. Epub 2019 Jun 28.
8
Helicobacter pylori-induced epithelial-mesenchymal transition, a potential role of gastric cancer initiation and an emergence of stem cells.幽门螺杆菌诱导的上皮-间质转化、在胃癌起始中的潜在作用及干细胞的出现
Carcinogenesis. 2015 May;36(5):553-63. doi: 10.1093/carcin/bgv022. Epub 2015 Mar 16.
9
Differential expression of the epithelial mesenchymal transition factors Snail, Slug, Twist, TGF-β, and E-cadherin in ameloblastoma.成釉细胞瘤中上皮-间质转化因子Snail、Slug、Twist、转化生长因子-β（TGF-β）和E-钙黏蛋白的差异表达
Med Mol Morphol. 2017 Jun;50(2):68-75. doi: 10.1007/s00795-016-0149-0. Epub 2016 Dec 19.
10
Endometriotic mesenchymal stem cells significantly promote fibrogenesis in ovarian endometrioma through the Wnt/β-catenin pathway by paracrine production of TGF-β1 and Wnt1.子宫内膜异位间充质干细胞通过旁分泌产生转化生长因子-β1（TGF-β1）和Wnt1，经Wnt/β-连环蛋白途径显著促进卵巢子宫内膜异位囊肿中的纤维生成。
Hum Reprod. 2016 Jun;31(6):1224-35. doi: 10.1093/humrep/dew058. Epub 2016 Mar 22.

引用本文的文献

1
Effects of Two Calcium Silicate Cements on Transforming Growth Factor-1 Secretion from Human Dental Pulp Stem Cells.两种硅酸钙水门汀对人牙髓干细胞转化生长因子-1分泌的影响
Iran Endod J. 2018 Fall;13(4):522-527. doi: 10.22037/iej.v13i4.21885.
2
Betulinic Acid Inhibits the Stemness of Gastric Cancer Cells by Regulating the GRP78-TGF-β1 Signaling Pathway and Macrophage Polarization.桦木酸通过调控 GRP78-TGF-β1 信号通路及巨噬细胞极化抑制胃癌干细胞的干性。
Molecules. 2023 Feb 11;28(4):1725. doi: 10.3390/molecules28041725.
3
The Expression of , , and miRNA-21 in the Ectopic and Eutopic Endometrium of Women with Endometriosis.

本文引用的文献

1
Activation of IL6/IGFIR confers poor prognosis of HBV-related hepatocellular carcinoma through induction of OCT4/NANOG expression.IL6/IGFIR 的激活通过诱导 OCT4/NANOG 表达赋予 HBV 相关肝细胞癌不良预后。
Clin Cancer Res. 2015 Jan 1;21(1):201-10. doi: 10.1158/1078-0432.CCR-13-3274.
2
BMP-7 blocks the effects of TGF-β-induced EMT in cholangiocarcinoma.骨形态发生蛋白-7可阻断转化生长因子-β诱导的胆管癌上皮-间质转化效应。
Tumour Biol. 2014 Oct;35(10):9667-76. doi: 10.1007/s13277-014-2246-9. Epub 2014 Jun 27.
3
Hypoxia inducible factor 2α/insulin-like growth factor receptor signal loop supports the proliferation and Oct-4 maintenance of mouse germline stem cells.
子宫内膜异位症患者异位和在位子宫内膜中 、 、miRNA-21 的表达。
Int J Mol Sci. 2023 Jan 26;24(3):2453. doi: 10.3390/ijms24032453.
4
Di-(2-ethylhexyl) Phthalate Triggers Proliferation, Migration, Stemness, and Epithelial-Mesenchymal Transition in Human Endometrial and Endometriotic Epithelial Cells via the Transforming Growth Factor-β/Smad Signaling Pathway.邻苯二甲酸二（2-乙基己基）酯通过转化生长因子-β/ Smad 信号通路触发人子宫内膜和子宫内膜异位症上皮细胞的增殖、迁移、干性和上皮-间充质转化。
Int J Mol Sci. 2022 Apr 1;23(7):3938. doi: 10.3390/ijms23073938.
5
Hepatitis B and Hepatitis C Virus Infection Promote Liver Fibrogenesis through a TGF-β1-Induced OCT4/Nanog Pathway.乙型肝炎和丙型肝炎病毒感染通过 TGF-β1 诱导的 OCT4/Nanog 通路促进肝纤维化。
J Immunol. 2022 Feb 1;208(3):672-684. doi: 10.4049/jimmunol.2001453. Epub 2022 Jan 12.
6
Controlling Semi-Invasive Activity of Human Endometrial Stromal Cells by Inhibiting NF-kB Signaling Pathway Using Aloe-emodin and Aspirin.通过使用芦荟大黄素和阿司匹林抑制NF-κB信号通路来控制人子宫内膜基质细胞的半侵袭活性
J Reprod Infertil. 2021 Oct-Dec;22(4):227-240. doi: 10.18502/jri.v22i4.7648.
7
Reprogramming oral epithelial keratinocytes into a pluripotent phenotype for tissue regeneration.将口腔上皮角质细胞重编程为多能表型以进行组织再生。
Clin Exp Dent Res. 2021 Dec;7(6):1112-1121. doi: 10.1002/cre2.455. Epub 2021 May 22.
8
The Role and Specific Mechanism of OCT4 in Cancer Stem Cells: A Review.OCT4在癌症干细胞中的作用及具体机制：综述
Int J Stem Cells. 2020 Nov 30;13(3):312-325. doi: 10.15283/ijsc20097.
9
LncRNA RHPN1-AS1 Targeting miR-625/REG3A Promotes Cell Proliferation And Invasion Of Glioma Cells.靶向miR-625/REG3A的长链非编码RNA RHPN1-AS1促进胶质瘤细胞的增殖和侵袭
Onco Targets Ther. 2019 Sep 26;12:7911-7921. doi: 10.2147/OTT.S209563. eCollection 2019.
10
Triple-Negative Breast Cancer: Current Understanding and Future Therapeutic Breakthrough Targeting Cancer Stemness.三阴性乳腺癌：当前认识与针对癌症干性的未来治疗突破
Cancers (Basel). 2019 Sep 9;11(9):1334. doi: 10.3390/cancers11091334.
缺氧诱导因子 2α/胰岛素样生长因子受体信号环路支持小鼠生殖干细胞的增殖和 Oct-4 维持。
Mol Hum Reprod. 2014 Jun;20(6):526-37. doi: 10.1093/molehr/gau016. Epub 2014 Mar 5.
4
Expression of the pluripotent transcription factor OCT4 promotes cell migration in endometriosis.多能转录因子 OCT4 的表达促进子宫内膜异位症中的细胞迁移。
Fertil Steril. 2013 Apr;99(5):1332-1339.e5. doi: 10.1016/j.fertnstert.2012.11.033. Epub 2013 Jan 3.
5
Targeting the TGFβ signalling pathway in disease.靶向疾病中的 TGFβ 信号通路。
Nat Rev Drug Discov. 2012 Oct;11(10):790-811. doi: 10.1038/nrd3810. Epub 2012 Sep 24.
6
Common chromosomal imbalances and stemness-related protein expression markers in endometriotic lesions from different anatomical sites: the potential role of stem cells.不同解剖部位子宫内膜异位症病灶中的常见染色体不平衡和干性相关蛋白表达标志物：干细胞的潜在作用。
Hum Reprod. 2012 Nov;27(11):3187-97. doi: 10.1093/humrep/des282. Epub 2012 Aug 30.
7
Regulation of EMT by TGFβ in cancer.TGFβ 对 EMT 的调控在癌症中的作用。
FEBS Lett. 2012 Jul 4;586(14):1959-70. doi: 10.1016/j.febslet.2012.02.037. Epub 2012 Feb 28.
8
Endometrial reconstruction from stem cells.干细胞子宫内膜重建。
Fertil Steril. 2012 Jul;98(1):11-20. doi: 10.1016/j.fertnstert.2012.05.004. Epub 2012 May 30.
9
TGF-β-induced epithelial-mesenchymal transition: a link between cancer and inflammation.TGF-β 诱导的上皮-间充质转化：癌症与炎症之间的联系。
Semin Cancer Biol. 2012 Oct;22(5-6):455-61. doi: 10.1016/j.semcancer.2012.05.004. Epub 2012 May 22.
10
Induction of epithelial-mesenchymal transition by transforming growth factor β.转化生长因子 β诱导上皮-间充质转化。
Semin Cancer Biol. 2012 Oct;22(5-6):446-54. doi: 10.1016/j.semcancer.2012.04.002. Epub 2012 Apr 23.