Evidence map›Paper›PMID 37452056›Full record

ArticleCell death discovery2023

Restricting epigenetic activity promotes the reprogramming of transformed cells to pluripotency in a line-specific manner.

Xiuling Fu, Qiang Zhuang, Isaac A Babarinde, Liyang Shi, Gang Ma, Haoqing Hu, Yuhao Li, Jiao Chen, Zhen Xiao, Boping Deng and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 6 citations in OpenAlex.

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  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 2 countries.

Xiuling FuDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Qiang ZhuangDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Isaac A BabarindeDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Liyang ShiDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Gang MaDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Haoqing HuSchool of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Yuhao LiDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Jiao ChenDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Zhen XiaoDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Boping DengDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Li SunDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Ralf JauchSchool of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.ORCID http://orcid.org/0000-0002-6590-9579
Andrew P HutchinsDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China. andrewh@sustech.edu.cn.ORCID http://orcid.org/0000-0001-7784-2255
Southern University of Science and Technology · CNUniversity of Hong Kong · HK

Funding

National Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint Fund (NSFC-Yunnan Joint Fund) 32150710521Shenzhen Science and Technology Innovation Commission ZDSYS20200811144002008
6 · The paper itself

Abstract

Somatic cell reprogramming and oncogenic transformation share surprisingly similar features, yet transformed cells are resistant to reprogramming. Epigenetic barriers must block transformed cells from reprogramming, but the nature of those barriers is unclear. In this study, we generated a systematic panel of transformed mouse embryonic fibroblasts (MEFs) using oncogenic transgenes and discovered transformed cell lines compatible with reprogramming when transfected with Oct4/Sox2/Klf4/Myc. By comparing the reprogramming-capable and incapable transformed lines we identified multiple stages of failure in the reprogramming process. Some transformed lines failed at an early stage, whilst other lines seemed to progress through a conventional reprogramming process. Finally, we show that MEK inhibition overcomes one critical reprogramming barrier by indirectly suppressing a hyperacetylated active epigenetic state. This study reveals that diverse epigenetic barriers underly resistance to reprogramming of transformed cells.

Identifiers

PMID37452056
PMCPMC10349098
OpenAlexW4384340199

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.