Evidence map›Paper›PMID 31811153›Full record

ArticleNature communications2019

Targeting of apoptosis gene loci by reprogramming factors leads to selective eradication of leukemia cells.

Yajie Wang, Ting Lu, Guohuan Sun, Yawei Zheng, Shangda Yang, Hongyan Zhang, Sha Hao, Yanfeng Liu, Shihui Ma, Houyu Zhang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Protein Engineering for Spatiotemporally Resolved Cellular Monitoring.Annual review of analytical chemistry (Palo Alto, Calif.) · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

15 authors at 3 institutions in 1 country.

Yajie WangState Key Laboratory of Experimental Hematology, Beijing, China.
Ting LuDepartment of Developmental Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Guohuan SunState Key Laboratory of Experimental Hematology, Beijing, China.
Yawei ZhengState Key Laboratory of Experimental Hematology, Beijing, China.
Shangda YangState Key Laboratory of Experimental Hematology, Beijing, China.
Hongyan ZhangState Key Laboratory of Experimental Hematology, Beijing, China.
Sha HaoState Key Laboratory of Experimental Hematology, Beijing, China.
Yanfeng LiuState Key Laboratory of Experimental Hematology, Beijing, China.
Shihui MaState Key Laboratory of Experimental Hematology, Beijing, China.
Houyu ZhangDepartment of Developmental Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Yongxin RuState Key Laboratory of Experimental Hematology, Beijing, China.
Shaorong GaoSchool of Life Sciences and Technology, Tongji University, Shanghai, China.
Kuangyu YenDepartment of Developmental Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. kuangyuyen@smu.edu.cn.
Hui ChengState Key Laboratory of Experimental Hematology, Beijing, China. chenghui@ihcams.ac.cn.
Tao ChengState Key Laboratory of Experimental Hematology, Beijing, China. chengtao@ihcams.ac.cn.ORCID http://orcid.org/0000-0003-4395-1095
Chinese Academy of Medical Sciences & Peking Union Medical College · CNSouthern Medical University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Applying somatic cell reprogramming strategies in cancer cell biology is a powerful approach to analyze mechanisms of malignancy and develop new therapeutics. Here, we test whether leukemia cells can be reprogrammed in vivo using the canonical reprogramming transcription factors-Oct4, Sox2, Klf4, and c-Myc (termed as OSKM). Unexpectedly, we discover that OSKM can eradicate leukemia cells and dramatically improve survival of leukemia-bearing mice. By contrast, OSKM minimally impact normal hematopoietic cells. Using ATAC-seq, we find OSKM induce chromatin accessibility near genes encoding apoptotic regulators in leukemia cells. Moreover, this selective effect also involves downregulation of H3K9me3 as an early event. Dissection of the functional effects of OSKM shows that Klf4 and Sox2 play dominant roles compared to c-Myc and Oct4 in elimination of leukemia cells. These results reveal an intriguing paradigm by which OSKM-initiated reprogramming induction can be leveraged and diverged to develop novel anti-cancer strategies.

Indexed as

AnimalsApoptosisBone MarrowCellular ReprogrammingChromatinGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksHEK293 CellsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsLeukemiaMiceMice, Inbred NODMice, SCIDChromatinKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsMyc protein, mouseOctamer Transcription Factor-3Proto-Oncogene Proteins c-mycSox2 protein, mouseSOXB1 Transcription Factors

Identifiers

PMID31811153
PMCPMC6898631
OpenAlexW2993603673

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.