• 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

PTPRK 通过直接抑制致癌 CD133 抑制结肠癌细胞的进展和化疗耐药性。

PTPRK suppresses progression and chemo-resistance of colon cancer cells via direct inhibition of pro-oncogenic CD133.

机构信息

Laboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, Japan.

Laboratory of Oncogenomics, Chiba Cancer Center Research Institute, Japan.

出版信息

FEBS Open Bio. 2019 May;9(5):935-946. doi: 10.1002/2211-5463.12636. Epub 2019 Apr 18.

DOI:10.1002/2211-5463.12636
PMID:30947381
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6487712/
Abstract

Receptor-type protein tyrosine phosphatase κ (PTPRK) is considered to be a candidate tumor suppressor. PTPRK dephosphorylates CD133, which is a stem cell marker; phosphorylated CD133 accelerates xenograft tumor growth of colon cancer cells through the activation of AKT, but the functional significance of this has remained elusive. In this study, we have demonstrated that knockdown of PTPRK potentiates the pro-oncogenic CD133-AKT pathway in colon cancer cells. Intriguingly, depletion of PTPRK significantly reduced sensitivity to the anti-cancer drug oxaliplatin and was accompanied by up-regulation of phosphorylation of Bad, a downstream target of AKT. Together, our present observations strongly suggest that the CD133-PTPRK axis plays a pivotal role in the regulation of colon cancer progression as well as drug resistance.

摘要

受体型蛋白酪氨酸磷酸酶 κ（PTPRK）被认为是一种候选肿瘤抑制因子。PTPRK 去磷酸化 CD133，CD133 是一种干细胞标记物；磷酸化的 CD133 通过激活 AKT 加速结肠癌细胞的异种移植肿瘤生长，但这一功能意义仍不清楚。在这项研究中，我们已经证明，PTPRK 的敲低增强了结肠癌细胞中致癌性的 CD133-AKT 通路。有趣的是，PTPRK 的耗竭显著降低了对抗癌药物奥沙利铂的敏感性，并伴随着 AKT 的下游靶标 Bad 的磷酸化上调。总之，我们目前的观察结果强烈表明，CD133-PTPRK 轴在调节结肠癌的进展以及耐药性方面起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/a9a7a566f82e/FEB4-9-935-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/31e74410bfd9/FEB4-9-935-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/351bb341049e/FEB4-9-935-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/e68d560827ca/FEB4-9-935-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/9b1d5f7a2787/FEB4-9-935-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/5ddc581fbd7f/FEB4-9-935-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/a9a7a566f82e/FEB4-9-935-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/31e74410bfd9/FEB4-9-935-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/351bb341049e/FEB4-9-935-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/e68d560827ca/FEB4-9-935-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/9b1d5f7a2787/FEB4-9-935-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/5ddc581fbd7f/FEB4-9-935-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cefc/6487712/a9a7a566f82e/FEB4-9-935-g006.jpg

相似文献

1
PTPRK suppresses progression and chemo-resistance of colon cancer cells via direct inhibition of pro-oncogenic CD133.PTPRK 通过直接抑制致癌 CD133 抑制结肠癌细胞的进展和化疗耐药性。
FEBS Open Bio. 2019 May;9(5):935-946. doi: 10.1002/2211-5463.12636. Epub 2019 Apr 18.
2
Receptor-type protein tyrosine phosphatase κ directly dephosphorylates CD133 and regulates downstream AKT activation.受体型蛋白酪氨酸磷酸酶κ直接使CD133去磷酸化并调节下游AKT激活。
Oncogene. 2015 Apr 9;34(15):1949-60. doi: 10.1038/onc.2014.141. Epub 2014 Jun 2.
3
Dual roles of protein tyrosine phosphatase kappa in coordinating angiogenesis induced by pro-angiogenic factors.蛋白酪氨酸磷酸酶κ在协调促血管生成因子诱导的血管生成中的双重作用。
Int J Oncol. 2017 Apr;50(4):1127-1135. doi: 10.3892/ijo.2017.3884. Epub 2017 Feb 20.
4
CD133-induced TM4SF5 expression promotes sphere growth via recruitment and blocking of protein tyrosine phosphatase receptor type F (PTPRF).CD133 诱导 TM4SF5 表达通过招募和阻断蛋白酪氨酸磷酸酶受体 F（PTPRF）促进球体生长。
Cancer Lett. 2018 Dec 1;438:219-231. doi: 10.1016/j.canlet.2018.09.009. Epub 2018 Sep 11.
5
Tumor derived mutations of protein tyrosine phosphatase receptor type k affect its function and alter sensitivity to chemotherapeutics in glioma.肿瘤中蛋白酪氨酸磷酸酯酶受体 k 的突变影响其功能，并改变胶质细胞瘤对化疗药物的敏感性。
PLoS One. 2013 May 16;8(5):e62852. doi: 10.1371/journal.pone.0062852. Print 2013.
6
Receptor-like protein tyrosine phosphatase κ negatively regulates the apoptosis of prostate cancer cells via the JNK pathway.受体样蛋白酪氨酸磷酸酶 κ 通过 JNK 通路负调控前列腺癌细胞的凋亡。
Int J Oncol. 2013 Nov;43(5):1560-8. doi: 10.3892/ijo.2013.2082. Epub 2013 Aug 29.
7
Receptor-type tyrosine-protein phosphatase κ directly targets STAT3 activation for tumor suppression in nasal NK/T-cell lymphoma.受体型酪氨酸蛋白磷酸酶 κ 通过直接靶向 STAT3 激活抑制鼻腔 NK/T 细胞淋巴瘤的肿瘤发生。
Blood. 2015 Mar 5;125(10):1589-600. doi: 10.1182/blood-2014-07-588970. Epub 2015 Jan 22.
8
Pancreatic Tumor Progression Associated With CD133 Overexpression: Involvement of Increased TERT Expression and Epidermal Growth Factor Receptor-Dependent Akt Activation.与CD133过表达相关的胰腺肿瘤进展：端粒酶逆转录酶（TERT）表达增加及表皮生长因子受体依赖性Akt激活的参与
Pancreas. 2016 Mar;45(3):443-57. doi: 10.1097/MPA.0000000000000460.
9
Notch and TGF-β pathways cooperatively regulate receptor protein tyrosine phosphatase-κ (PTPRK) gene expression in human primary keratinocytes.Notch和TGF-β信号通路协同调节人原代角质形成细胞中受体蛋白酪氨酸磷酸酶κ（PTPRK）基因的表达。
Mol Biol Cell. 2015 Mar 15;26(6):1199-206. doi: 10.1091/mbc.E14-12-1591. Epub 2015 Jan 21.
10
PTPRK negatively regulates transcriptional activity of wild type and mutated oncogenic beta-catenin and affects membrane distribution of beta-catenin/E-cadherin complexes in cancer cells.蛋白酪氨酸磷酸酶受体K（PTPRK）负向调节野生型和突变型致癌β-连环蛋白的转录活性，并影响癌细胞中β-连环蛋白/E-钙黏蛋白复合物的膜分布。
Cell Signal. 2008 May;20(5):872-83. doi: 10.1016/j.cellsig.2007.12.024. Epub 2008 Jan 12.

引用本文的文献

1
Protein tyrosine phosphatase receptor type kappa (PTPRK) revisited: evolving insights into structure, function, and pathology.蛋白酪氨酸磷酸酶κ型受体（PTPRK）再探讨：对其结构、功能及病理学的新认识
J Transl Med. 2025 May 12;23(1):534. doi: 10.1186/s12967-025-06496-1.
2
The receptor protein tyrosine phosphatase PTPRK promotes intestinal repair and catalysis-independent tumour suppression.受体蛋白酪氨酸磷酸酶 PTPRK 促进肠道修复和非催化依赖性肿瘤抑制。
J Cell Sci. 2024 Jul 15;137(14). doi: 10.1242/jcs.261914. Epub 2024 Jul 22.
3
Emerging roles of prominin-1 (CD133) in the dynamics of plasma membrane architecture and cell signaling pathways in health and disease.

本文引用的文献

1
Multi-organ Mapping of Cancer Risk.癌症风险的多器官图谱
Cell. 2016 Aug 25;166(5):1132-1146.e7. doi: 10.1016/j.cell.2016.07.045.
2
Novel Implications of DNA Damage Response in Drug Resistance of Malignant Cancers Obtained from the Functional Interaction between p53 Family and RUNX2.p53家族与RUNX2功能相互作用对恶性肿瘤耐药性的DNA损伤反应新影响
Biomolecules. 2015 Oct 23;5(4):2854-76. doi: 10.3390/biom5042854.
3
First-line chemotherapy for mCRC—a review and evidence-based algorithm.mCRC 的一线化疗——综述与循证算法。
Prominin-1（CD133）在健康和疾病中参与质膜结构和细胞信号通路动态变化的新兴作用。
Cell Mol Biol Lett. 2024 Mar 26;29(1):41. doi: 10.1186/s11658-024-00554-0.
4
Functional Roles of CD133: More than Stemness Associated Factor Regulated by the Microenvironment.CD133 的功能作用：不只是微环境调控的干性相关因子
Stem Cell Rev Rep. 2024 Jan;20(1):25-51. doi: 10.1007/s12015-023-10647-6. Epub 2023 Nov 3.
5
The Impact of and Polymorphisms on the Preeclampsia Risk in Han Chinese Women.[基因名称]多态性对汉族女性子痫前期风险的影响。 （你提供的原文中“and”前后应该有具体的基因名称等内容缺失，我按照补充完整后的大致意思翻译了，你可根据实际情况修改完善）
Int J Hypertens. 2021 Oct 4;2021:3275081. doi: 10.1155/2021/3275081. eCollection 2021.
6
CD133 prevents colon cancer cell death induced by serum deprivation through activation of Akt-mediated protein synthesis and inhibition of apoptosis.CD133 通过激活 Akt 介导的蛋白质合成和抑制细胞凋亡来防止血清剥夺诱导的结肠癌细胞死亡。
FEBS Open Bio. 2021 May;11(5):1382-1394. doi: 10.1002/2211-5463.13145. Epub 2021 Mar 28.
7
B7-H3 Induces Ovarian Cancer Drugs Resistance Through An PI3K/AKT/BCL-2 Signaling Pathway.B7-H3通过PI3K/AKT/BCL-2信号通路诱导卵巢癌耐药。
Cancer Manag Res. 2019 Dec 3;11:10205-10214. doi: 10.2147/CMAR.S222224. eCollection 2019.
Nat Rev Clin Oncol. 2015 Oct;12(10):607-19. doi: 10.1038/nrclinonc.2015.129. Epub 2015 Jul 28.
4
Cancer statistics, 2015.癌症统计数据，2015 年。
CA Cancer J Clin. 2015 Jan-Feb;65(1):5-29. doi: 10.3322/caac.21254. Epub 2015 Jan 5.
5
Receptor-type protein tyrosine phosphatase κ directly dephosphorylates CD133 and regulates downstream AKT activation.受体型蛋白酪氨酸磷酸酶κ直接使CD133去磷酸化并调节下游AKT激活。
Oncogene. 2015 Apr 9;34(15):1949-60. doi: 10.1038/onc.2014.141. Epub 2014 Jun 2.
6
3D cell culture systems modeling tumor growth determinants in cancer target discovery.三维细胞培养系统模拟肿瘤生长决定因素在癌症靶点发现中的作用。
Adv Drug Deliv Rev. 2014 Apr;69-70:29-41. doi: 10.1016/j.addr.2014.03.001. Epub 2014 Mar 15.
7
Generation of prostate tumor-initiating cells is associated with elevation of reactive oxygen species and IL-6/STAT3 signaling.前列腺肿瘤起始细胞的产生与活性氧和 IL-6/STAT3 信号的升高有关。
Cancer Res. 2013 Dec 1;73(23):7090-100. doi: 10.1158/0008-5472.CAN-13-1560. Epub 2013 Oct 7.
8
DNA methylation of membrane-bound tyrosine phosphatase genes in acute lymphoblastic leukaemia.急性淋巴细胞白血病中膜结合酪氨酸磷酸酶基因的 DNA 甲基化。
Leukemia. 2014 Apr;28(4):787-93. doi: 10.1038/leu.2013.270. Epub 2013 Sep 18.
9
Receptor-like protein tyrosine phosphatase κ negatively regulates the apoptosis of prostate cancer cells via the JNK pathway.受体样蛋白酪氨酸磷酸酶 κ 通过 JNK 通路负调控前列腺癌细胞的凋亡。
Int J Oncol. 2013 Nov;43(5):1560-8. doi: 10.3892/ijo.2013.2082. Epub 2013 Aug 29.
10
Tumor derived mutations of protein tyrosine phosphatase receptor type k affect its function and alter sensitivity to chemotherapeutics in glioma.肿瘤中蛋白酪氨酸磷酸酯酶受体 k 的突变影响其功能，并改变胶质细胞瘤对化疗药物的敏感性。
PLoS One. 2013 May 16;8(5):e62852. doi: 10.1371/journal.pone.0062852. Print 2013.