文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期,新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
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
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
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 @ 2025

OCT4 作为 miR-34a 的靶标,可刺激 p63 但抑制 p53,从而促进人细胞转化。

OCT4 as a target of miR-34a stimulates p63 but inhibits p53 to promote human cell transformation.

机构信息

Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, USA.

Division of Space Life Sciences, Universities Space Research Association, Houston, TX, USA.

出版信息

Cell Death Dis. 2014 Jan 23;5(1):e1024. doi: 10.1038/cddis.2013.563.


DOI:10.1038/cddis.2013.563
PMID:24457968
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4040665/
Abstract

Human cell transformation is a key step for oncogenic development, which involves multiple pathways; however, the mechanism remains unclear. To test our hypothesis whether cell oncogenic transformation shares some mechanisms with the process of reprogramming non-stem cells to induced pluripotent stem cells (iPSC), we studied the relationship among the key factors for promoting or inhibiting iPSC in radiation-transformed human epithelial cell lines derived from different tissues (lung, breast and colon). We unexpectedly found that p63 and OCT4 were highly expressed (accompanied by low expressed p53 and miR-34a) in all transformed cell lines examined when compared with their non-transformed counterparts. We further elucidated the relationship of these factors: the 3p strand of miR-34a directly targeted OCT4 by binding to the 3' untranslated region (3'-UTR) of OCT4 and, OCT4, in turn, stimulated p63 but inhibited p53 expression by binding to a specific region of the p63 or p53 promoter. Moreover, we revealed that the effects of OCT4 on promoting cell oncogenic transformation were by affecting p63 and p53. These results support that a positive loop exists in human cells: OCT4 upregulation as a consequence of inhibition of miR-34a, promotes p63 but suppresses p53 expression, which further stimulates OCT4 upregulation by downregulating miR-34a. This functional loop contributes significantly to cell transformation and, most likely, also to the iPSC process.

摘要

人类细胞转化是致癌发展的关键步骤,涉及多个途径;然而,其机制尚不清楚。为了验证我们的假设,即细胞致癌转化是否与将非干细胞重编程为诱导多能干细胞(iPSC)的过程共享一些机制,我们研究了促进或抑制源自不同组织(肺、乳腺和结肠)的辐射转化人上皮细胞系中 iPSC 的关键因素之间的关系。我们出人意料地发现,与未转化的细胞相比,所有转化细胞系中 p63 和 OCT4 的表达水平均升高(同时伴有低表达的 p53 和 miR-34a)。我们进一步阐明了这些因素之间的关系:miR-34a 的 3p 链通过与 OCT4 的 3'非翻译区(3'-UTR)结合而直接靶向 OCT4,而 OCT4 则通过结合 p63 或 p53 启动子的特定区域来刺激 p63 但抑制 p53 表达。此外,我们揭示了 OCT4 对促进细胞致癌转化的影响是通过影响 p63 和 p53 实现的。这些结果支持人细胞中存在正反馈环:miR-34a 抑制的结果是 OCT4 的上调,促进了 p63 的表达,但抑制了 p53 的表达,这进一步通过下调 miR-34a 来刺激 OCT4 的上调。这个功能环对细胞转化有重要贡献,很可能对 iPSC 过程也有重要贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/7d6e9b9f17ed/cddis2013563f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/623f6d2eb263/cddis2013563f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/b310f3dafb23/cddis2013563f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/4311b9612019/cddis2013563f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/e38bccdc8703/cddis2013563f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/7d6e9b9f17ed/cddis2013563f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/623f6d2eb263/cddis2013563f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/b310f3dafb23/cddis2013563f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/4311b9612019/cddis2013563f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/e38bccdc8703/cddis2013563f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3768/4040665/7d6e9b9f17ed/cddis2013563f5.jpg

相似文献

[1]
OCT4 as a target of miR-34a stimulates p63 but inhibits p53 to promote human cell transformation.

Cell Death Dis. 2014-1-23

[2]
miR-34 miRNAs provide a barrier for somatic cell reprogramming.

Nat Cell Biol. 2011-10-23

[3]
MicroRNA-302 increases reprogramming efficiency via repression of NR2F2.

Stem Cells. 2013-2

[4]
Oct4/Sox2-regulated miR-302 targets cyclin D1 in human embryonic stem cells.

Mol Cell Biol. 2008-10

[5]
MiR-138 promotes induced pluripotent stem cell generation through the regulation of the p53 signaling.

Stem Cells. 2012-8

[6]
Critical regulation of miR-200/ZEB2 pathway in Oct4/Sox2-induced mesenchymal-to-epithelial transition and induced pluripotent stem cell generation.

Proc Natl Acad Sci U S A. 2013-2-5

[7]
Human fibroblast reprogramming to pluripotent stem cells regulated by the miR19a/b-PTEN axis.

PLoS One. 2014-4-16

[8]
Δ133p53 represses p53-inducible senescence genes and enhances the generation of human induced pluripotent stem cells.

Cell Death Differ. 2017-6

[9]
p53 regulates cell cycle and microRNAs to promote differentiation of human embryonic stem cells.

PLoS Biol. 2012-2-28

[10]
miR-129 targets CDK1 and iASPP to modulate Burkitt lymphoma cell proliferation in a TAp63-dependent manner.

J Cell Biochem. 2018-8-13

引用本文的文献

[1]
E47 upregulates ΔNp63α to promote growth of squamous cell carcinoma.

Cell Death Dis. 2021-4-8

[2]
Analysis of the Transcriptome: Regulation of Cancer Stemness in Breast Ductal Carcinoma by Vitamin D Compounds.

Cancer Prev Res (Phila). 2020-8

[3]
Transcription Factor and miRNA Interplays Can Manifest the Survival of ccRCC Patients.

Cancers (Basel). 2019-10-28

[4]
ERα is required for suppressing OCT4-induced proliferation of breast cancer cells via DNMT1/ISL1/ERK axis.

Cell Prolif. 2019-4-22

[5]
Ionizing radiation-induced growth in soft agar is associated with miR-21 upregulation in wild-type and DNA double strand break repair deficient cells.

DNA Repair (Amst). 2019-3-23

[6]
Rhamnetin induces apoptosis in human breast cancer cells via the miR-34a/Notch-1 signaling pathway.

Oncol Lett. 2019-1

[7]
The effects of ultrasound exposure on P-glycoprotein-mediated multidrug resistance in vitro and in vivo.

J Exp Clin Cancer Res. 2018-9-19

[8]
OCT4B regulates p53 and p16 pathway genes to prevent apoptosis of breast cancer cells.

Oncol Lett. 2018-7

[9]
Cardamonin reduces chemotherapy resistance of colon cancer cells via the TSP50/NF-κB pathway .

Oncol Lett. 2018-6

[10]
Decoding the Emerging Patterns Exhibited in Non-coding RNAs Characteristic of Lung Cancer with Regard to their Clinical Significance.

Curr Genomics. 2018-5

本文引用的文献

[1]
miRNA profiling of cancer.

Curr Opin Genet Dev. 2013-3-4

[2]
ΔNp63α represses anti-proliferative genes via H2A.Z deposition.

Genes Dev. 2012-9-26

[3]
miRNA-34 prevents cancer initiation and progression in a therapeutically resistant K-ras and p53-induced mouse model of lung adenocarcinoma.

Cancer Res. 2012-9-10

[4]
Loss of p63 and its microRNA-205 target results in enhanced cell migration and metastasis in prostate cancer.

Proc Natl Acad Sci U S A. 2012-9-4

[5]
MicroRNA-21 modulates the levels of reactive oxygen species by targeting SOD3 and TNFα.

Cancer Res. 2012-7-25

[6]
miR-34a functions as a tumor suppressor modulating EGFR in glioblastoma multiforme.

Oncogene. 2012-5-14

[7]
p53 regulates cell cycle and microRNAs to promote differentiation of human embryonic stem cells.

PLoS Biol. 2012-2-28

[8]
miR-34 miRNAs provide a barrier for somatic cell reprogramming.

Nat Cell Biol. 2011-10-23

[9]
Generation of tumor-initiating cells by exogenous delivery of OCT4 transcription factor.

Breast Cancer Res. 2011-9-27

[10]
Residual embryonic cells as precursors of a Barrett's-like metaplasia.

Cell. 2011-6-24

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

推荐工具

医学文档翻译智能文献检索