Evidence map›Paper›PMID 25088197›Full record

ArticleOncogene2015

Regulation of p21 by TWIST2 contributes to its tumor-suppressor function in human acute myeloid leukemia.

X Zhang, W Ma, J Cui, H Yao, H Zhou, Y Ge, L Xiao, X Hu, B-H Liu, J Yang and 5 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. miR-181a plays the tumor-suppressor role in chronic myeloid leukemia CD34Cellular and molecular life sciences : CMLS · 2023
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Up-regulation ofCell cycle (Georgetown, Tex.) · 2019
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. 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 4 institutions in 2 countries.

X Zhang1] Cyrus Tang Hematology Center, Soochow University, Suzhou, People's Republic of China [2] Collaborative Innovation Center of Hematology, Soochow University, Suzhou, People's Republic of China.
W Ma1] Cyrus Tang Hematology Center, Soochow University, Suzhou, People's Republic of China [2] Collaborative Innovation Center of Hematology, Soochow University, Suzhou, People's Republic of China.
J Cui1] Cyrus Tang Hematology Center, Soochow University, Suzhou, People's Republic of China [2] The First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Key Laboratory of Thrombosis and Hemostasis, Suzhou, People's Republic of China.
H Yao1] Cyrus Tang Hematology Center, Soochow University, Suzhou, People's Republic of China [2] The First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Key Laboratory of Thrombosis and Hemostasis, Suzhou, People's Republic of China.
H ZhouThe First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Key Laboratory of Thrombosis and Hemostasis, Suzhou, People's Republic of China.
Y GeCyrus Tang Hematology Center, Soochow University, Suzhou, People's Republic of China.
L XiaoCyrus Tang Hematology Center, Soochow University, Suzhou, People's Republic of China.
X HuThe First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Key Laboratory of Thrombosis and Hemostasis, Suzhou, People's Republic of China.
B-H LiuShanghai Center for Bioinformation Technology, Shanghai, People's Republic of China.
J YangShanghai Center for Bioinformation Technology, Shanghai, People's Republic of China.
Y-Y LiShanghai Center for Bioinformation Technology, Shanghai, People's Republic of China.
S Chen1] Collaborative Innovation Center of Hematology, Soochow University, Suzhou, People's Republic of China [2] The First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Key Laboratory of Thrombosis and Hemostasis, Suzhou, People's Republic of China.
C J EavesTerry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.
D Wu1] Collaborative Innovation Center of Hematology, Soochow University, Suzhou, People's Republic of China [2] The First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Key Laboratory of Thrombosis and Hemostasis, Suzhou, People's Republic of China.
Y Zhao1] Cyrus Tang Hematology Center, Soochow University, Suzhou, People's Republic of China [2] Collaborative Innovation Center of Hematology, Soochow University, Suzhou, People's Republic of China.
Soochow University · CNFirst Affiliated Hospital of Soochow University · CNShanghai Center For Bioinformation Technology · CNBC Cancer Agency · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TWIST2 has a dual function in tumors. Its implication in the initiation and metastasis of various solid tumors is well established, and its tumor-suppressor role in murine osteosarcoma cells has been reported recently. However, the function of TWIST2 and its underlying mechanisms in human normal and malignant hematopoiesis remain unclear. In the present study, we found that TWIST2 directly regulated p21 in human hematopoietic cells and whose silence promoted cell proliferation and cell cycle progression. Hypermethylation of TWIST2 occurred to 23 out of the 75 adult acute myeloid leukemia (AML) patients and resulted in the impaired expression of both TWIST2 and p21. Conversely, TWIST2 overexpression inhibited the growth of AML cells partially through its direct activation of p21 with intact HLH (helix-loop-helix) domain. The microarray data and gene expression validation showed that TWIST2 was sufficient to activate known tumor-suppressor genes, whereas suppress known oncogenes, which further supported its inhibitory effect against AML cells. Taken together, our data have identified a novel TWIST2-p21 axis that modulates the cell cycle of both normal and leukemic cells and demonstrated that the direct regulation of p21 by TWIST2 has a role in its tumor-suppressor function in AML.

Indexed as

AnimalsCell CycleCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21DNA MethylationGene Expression ProfilingGene Expression Regulation, NeoplasticHEK293 CellsHematopoietic Stem CellsHumansLeukemia, Myeloid, AcuteMiceNeoplasm TransplantationOligonucleotide Array Sequence AnalysisRepressor ProteinsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Repressor ProteinsTWIST2 protein, humanTwist-Related Protein 1

Identifiers

PMID25088197
OpenAlexW2029861523

What OpenQuestion holds

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Registered trials

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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.